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127 publications mentioning hsa-mir-342 (showing top 100)

Open access articles that are associated with the species Homo sapiens and mention the gene name mir-342. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

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[+] score: 441
In each cell line we observed a concordance between the levels of EVL expression and miR-342 expression (Figure 1C) suggesting that miR-342 expression is directly coupled to expression of EVL. [score:10]
The microarray data was validated by performing qRT-PCR of three miR-342 predicted target genes (SEMAD, BMP7, GEMIN4) and TXNIP (Figure 5D) which is not a predicted miR-342 target gene but highly upregulated in miR-342 expressing MCF-7/HER2Δ16 cells. [score:10]
Luciferase expression from the 3' UTR sequences of GEMIN4 and BMP7 was suppressed when coexpressed with miR-342 by 40 and 50%, respectively, suggesting that these genes are direct targets of miR-342 (Figure 5E). [score:10]
Although in situ methods for the detection of miRNA expression are not in clinical use, the fact that miR-342 expression is tightly correlated to its host gene EVL in multiple tumor cell mo dels [24, 33] including our breast tumor cell lines, provides a unique opportunity to use EVL mRNA expression as a surrogate marker for miR-342 expression in breast cancer patients. [score:9]
In order to identify potential direct and indirect targets of miR-342 we stably restored miR-342 levels in the tamoxifen resistant MCF-7/HER2Δ16 cell line and performed a gene expression analysis comparing vector control to miR-342 expressing MCF-7/HER2Δ16 cell clones. [score:9]
In this context, the miR-342 indirect target thioredoxin-interacting protein (TXNIP) is the most dramatically upregulated gene in response to miR-342 expression and could potentially mediate miR-342 action. [score:9]
Towards the goal of identifying direct and indirect targets of miR-342 we restored miR-342 expression in MCF-7/HER2Δ16 cells and analyzed changes in global gene expression by microarray. [score:9]
By these criteria miR-342 expressing MCF-7/HER2Δ16 cells showed differential expression of 160 genes, 13 of which are bioinformatically predicted to be direct targets of miR-342 (Table 2). [score:8]
Interestingly, the majority of predicted target genes were up-regulated by miR-342 expression. [score:8]
To determine if modulation of miR-342 expression impacts tamoxifen response we first suppressed miR-342 expression in the tamoxifen sensitive MCF-7/pcDNA and MCF-7/HER2 cell lines. [score:7]
Although these results are compelling, TXNIP is an upregulated indirect target of miR-342 and deciphering the interplay between miR-342 and TXNIP has proved difficult. [score:7]
Interestingly, 7 of these 13 genes were upregulated in the miR-342 expressing MCF-7/HER2Δ16 cells (Table 2). [score:6]
Expression of miR-342 was also reduced in a panel of tamoxifen refractory human breast tumors, underscoring the potential clinical importance of miR-342 downregulation. [score:6]
A direct gene target of miR-342 remains to be experimentally confirmed and bioinformatics reveals over 1000 potential miR-342 targets. [score:6]
Suppression of miR-342 Expression Promotes Tamoxifen Resistance. [score:5]
Most relevant to breast cancer is the suppression of pathway member cyclin B1 in miR-342 expressing MCF-7/HER2Δ16 cells. [score:5]
Interestingly, the two tamoxifen sensitive MCF-7/pcDNA and MCF-7/HER2 cell lines [12, 15] expressed high levels of miR-342 whereas the tamoxifen resistant MCF-7/HER2Δ16 [12, 15], TAMR1 [17], and LCC2 [16] cell lines all exhibited dramatically suppressed levels of miR-342 (Figure 1A). [score:5]
In colorectal cancer cells EVL/miR-342 expression is suppressed through hypermethylation of the EVL promoter [24]. [score:5]
Indicated fold changes in miR-342 expression were obtained from the qRT-PCR from E. Levels of miR-342-3p and miR-342-5p expression in MCF-7/HER2Δ16 cell lines. [score:5]
Although we could not identify an obvious association between the direct targets of miR-342 and tumor cell response to tamoxifen, Ingenuity Pathway Analysis of the entire set of genes significantly altered by miR-342 revealed a highly significant association of miR-342 regulated genes with cell apoptosis. [score:5]
Importantly, expression of miR-342-5p was between 10-80 fold lower than miR-342-3p and in many cases miR-342-5p expression was at the limits of qRT-PCR sensitivity (Additional File 1). [score:5]
Restoring miR-342 expression may represent a novel therapeutic approach to sensitizing and suppressing the growth of tamoxifen refractory breast tumors. [score:5]
miR-342 Expression is Suppressed in Primary Breast Tumors Associated with Tamoxifen Failure. [score:5]
Significantly, ERα(+) breast tumors that fail tamoxifen therapy with rapid recurrence within 3 years have significantly lower EVL expression levels [34], providing compelling support for the hypothesis that miR-342 suppression promotes tamoxifen resistance. [score:5]
Figure 1 Expression of miR-342 is suppressed in tamoxifen resistant breast tumor cells. [score:5]
Indicated fold changes in miR-342 expression were obtained from the qRT-PCR from E. Click here for file Levels of miR-342-3p and miR-342-5p expression in MCF-7/HER2Δ16 cell lines. [score:5]
To determine if miR-342 expression sensitizes breast tumor cells to tamoxifen therapy, we reintroduced miR-342 expression into the tamoxifen resistant MCF-7/HER2Δ16 and TAMR1 cell lines. [score:5]
The impact of miR-342 on gene expression in MCF-7/HER2Δ16 cells was not limited to miR-342 in silica predicted targets. [score:5]
Figure 5 Stable miR-342 expression alters gene expression and sensitizes MCF-7/HER2Δ16 cells to tamoxifen. [score:5]
Thus, in addition to a role in apoptosis, our results suggest that miR-342 may also influence multiple stages of the cell cycle through cyclin B1 suppression, multiple BRCA1 activities, p53 cell cycle checkpoint function, and PTEN tumor suppressor activity. [score:5]
These results suggest that expression of miR-342 sensitizes breast tumor cells to tamoxifen treatment and tamoxifen resistance can be acquired through suppression of miR-342. [score:5]
MCF-7 cells were transfected with 20 nM of hsa-miR-342-3p (Ambion) or pre-miR negative control (Ambion) followed by pMir target firefly luciferase reporter plasmid containing 3' UTR sequences from BMP7 or GEMIN4 (Origene) and a renilla luciferase expression vector. [score:5]
As an approach to the identification of miR-342 targets we examined transcriptome changes in miR-342 overexpressing cells by microarray analysis. [score:5]
Each cell line plated at 3000 cells per well in a 96-well tissue culture plate was cultured for 24 hrs in CS-MEM and then transfected with 50 nM of miRIDIAN miRNA inhibitor non-specific control 1 or miRIDIAN miRNA inhibitor hsa-miR-342-3p (Dharmacon) using Hyperfect Reagent (Qiagen) according to the manufacturer's instructions. [score:5]
Mining of archived microarray data revealed that EVL expression is significantly associated with ERα(+) breast tumors [25- 27] which is consistent with recent studies reporting a strong correlation between ERα and miR-342 expression [23]. [score:5]
miR-342 Expression is Suppressed in Tamoxifen Resistant Breast Tumor Cells. [score:5]
Figure 2 Expression of miR-342 is suppressed in primary breast tumors associated with tamoxifen failure. [score:5]
Our results suggest that miR-342 expression and/or expression of the surrogate marker EVL may emerge as important breast tumor markers predicting clinical response to tamoxifen intervention. [score:5]
Differentially regulated genes in miR-342 -expressing MCF-7/HER2Δ16 cells were defined as those with at least 1.5-fold change (p < 0.05) compared to vector expressing cells (Figure 5C). [score:5]
MCF-7/HER2Δ16 cells stably transfected with an expression vector containing the hsa-miR-342-3p precursor sequence (miR-342), resulted in an approximate 7-fold increase in miR-342 levels when compared to the parental MCF-7/HER2Δ16 cell line (Figure 4A) with undetectable levels of miR-342-5p expression (Additional File 3). [score:4]
Our findings suggest that miR-342 regulates tamoxifen response in breast tumor cell lines and our clinical data indicates a trend towards reduced miR-342 expression and tamoxifen resistance. [score:4]
Here we show that deregulation of miR-342 contributes to tamoxifen resistance in multiple mo dels of tamoxifen resistance including the HER2Δ16 overexpression mo del. [score:4]
In addition, our results suggest that miR-342 regulates expression of genes involved in tamoxifen mediated tumor cell apoptosis and cell cycle progression. [score:4]
Specifically, we demonstrate that miR-342 is downregulated in tamoxifen resistant breast tumor cell lines and tamoxifen refractory human breast tumors. [score:4]
In corroboration with recent findings that deregulation of miRNAs contributes to the acquisition of anti-estrogen resistance [11- 13], we show that miR-342, which is suppressed in tamoxifen resistant cells, is associated with increased tamoxifen sensitivity of breast tumor cells. [score:4]
To determine if miR-342 downregulation was associated with clinical tamoxifen failure, we used DIG-labeled LNA modified miRNA probes to detect miR-342 in primary human breast tumors by ISH and independently scored each tumor on a scale of 0-3 with 3 being the most intense miR-342 staining (Additional File 2 and Figure 2A, B). [score:4]
Accordingly, IPA analysis identified miR-342 regulated genes significantly represented in multiple pathways that directly regulate breast tumor cell cycle progression including cyclin B1, p53, and BRCA1. [score:4]
As a global approach to identifying miR-342 target genes we performed gene expression profiling of MCF-7/HER2Δ16 stably transfected with miR-342 compared to vector control cells on a HuGene 1.0 Affymetrix microarray platform. [score:4]
We observed significant and dramatic downregulation of miR-342 in the MCF-7/HER2Δ16 cell line as well as the HER2 negative but tamoxifen resistant MCF-7 variants TAMR1 and LCC2. [score:4]
We observed significant alteration of 13 genes predicted by bioinformatics to be miR-342 targets. [score:3]
In breast cancer independent studies have shown that similar to EVL, expression of miR-342 is associated with ERα(+) breast tumors http://www. [score:3]
File shows qRT-PCR data comparing levels of miR-342-3p and miR-342-5p expression in MCF-7/HER2Δ16 stable cell lines. [score:3]
Each section was scored by comparing staining intensity of stably expressing miR-342 MCF-7/HER2Δ16 cells given a score of 3 and the MCF-7/HER2Δ16 cells with a score of 0 to the staining of tumor cells present in each section. [score:3]
This result is consistent with our observation that ectopic miR-342 expression sensitized tamoxifen resistant cells to tamoxifen -induced apoptosis. [score:3]
CS-FBS MEM: charcoal stripped fetal bovine serum in phenol red free MEM; E2: 17-β-estradiol; ERα: estrogen receptor alpha; EVL: Ena/Vasp-like; FFPE: formalin fixed paraffin embedded; HER2Δ16: oncogenic splice isoform of HER2; IPA: ingenuity pathway analysis; ISH: in situ hybridization; miRNA: micro RNA; miRNAs: micro RNAs; miR-342: miR-342-3p; MTT: 3-(4,5-dimethylthiazol-2-yl])-2,5-diphenyltetrazolium bromide; PI: propidium iodine; qRT-PCR: quantitative reverse transcriptase polymerase chain reaction; TAM: 4-hydroxytamoxifen; TXNIP: thioredoxin-interacting protein; UTR: untranslated region The authors declare that they have no competing interests. [score:3]
Levels of miR-342-3p and miR-342-5p expression in breast tumor cell lines. [score:3]
Restoration of miR-342 expression in tamoxifen-resistant MCF-7/HER2Δ16 and TAMR1 cells sensitized both cell lines to tamoxifen treatment with a significant reduction in cell growth (Figure 4A) and significant increase in tamoxifen -induced apoptosis (Figure 4B). [score:3]
Total RNA was isolated from each cell line and miR-342-3p or miR-342-5p expression levels relative to GAPDH were analyzed by qRT-PCR. [score:3]
File shows qRT-PCR data comparing levels of miR-342-3p and miR-342-5p expression in experimental cell lines. [score:3]
Click here for file Scoring of miR-342 expression by ISH in primary breast tumors and breast tumor cell lines. [score:3]
We first determined if loss of miR-342 was a common feature of tamoxifen resistance by comparing miR-342 expression by northern blot in multiple tamoxifen sensitive and resistant MCF-7 variants. [score:3]
We further demonstrate that miR-342-3p (miR-342), an ERα associated miRNA [23], was dramatically suppressed in multiple tamoxifen resistant breast tumor cell lines and in primary breast tumors of patients who failed tamoxifen therapy. [score:3]
A dramatic increase in the number of PI positive (dead cells) was observed in response to tamoxifen treatment but only in cells where miR-342 expression was restored (Figure 4C). [score:3]
Figure 3 Suppression of miR-342 promotes tamoxifen resistance. [score:3]
File contains controls for ISH showing different levels of miR-342 expression and ISH scoring. [score:3]
Similarly, miR-342 expression in colorectal cancer cells results in tumor cell apoptosis [24]. [score:3]
To generate the miR-342 expressing MCF-7/HER2Δ16 cell line a 342 bp sequence containing the pre-miR-342 sequence (GRCh37:14:100575892:100576190:1) flanked by 100 bp upstream and downstream was prepared as a minigene (Integrated DNA Technologies) and subcloned into pCMV-puro-silencer (Ambion). [score:3]
Scoring of miR-342 expression by ISH in primary breast tumors and breast tumor cell lines. [score:3]
Total RNA was isolated from each cell line and miR-342-3p or miR-342-5p expression levels relative to RNU44 were analyzed by qRT-PCR. [score:3]
With the potential of miRNA therapy, restoring miR-342 expression may constitute a novel therapeutic strategy to sensitize endocrine refractory breast tumors. [score:3]
Bioinformatic analyses predict that miR-342 can target between 169 to 1069 different genes. [score:3]
Restored miR-342 Expression Sensitizes Resistant Breast Tumor Cells to Tamoxifen. [score:3]
Transient transfection of each cell line with a miR-342 inhibitor promoted partial but significant tamoxifen resistance (p < 0.01) with a significant decrease in tamoxifen induced apoptosis (p < 0.005)(Figure 3). [score:3]
Click here for file Levels of miR-342-3p and miR-342-5p expression in breast tumor cell lines. [score:3]
As predicted, restoration of miR-342 expression sensitized MCF-7/HER2Δ16 cells to tamoxifen (Figure 5B). [score:3]
Taken together these results implicate miR-342 expression as an important mediator of tamoxifen induced apoptosis in breast tumor cells. [score:3]
Data represents mean +/- SE percent inhibition of luciferase activity of miR-342 transfected cells relative to pre-miR negative control. [score:3]
org[23, 25- 27] further supporting co -expression of miR-342 with EVL in ERα(+) tumors. [score:3]
With the exception of the tamoxifen sensitive MCF-7/HER2 cells, treatment with E2 alone or in combination with TAM did not significantly alter miR-342 expression (Figure 1B). [score:3]
Inhibition of miR-342. [score:3]
Transient Expression of miR-342. [score:3]
Expression of miR-342 was quantitated by qRT-PCR from total RNA exactly as described elsewhere [12]. [score:3]
Restoring miR-342 expression in the MCF-7/HER2Δ16 and TAMR1 cell lines sensitized these cells to tamoxifen -induced apoptosis with a dramatic reduction in cell growth. [score:3]
Levels of miR-342-5p expression were at the lower limits of qRT-PCR sensitivity. [score:3]
The samples are scored as (A) 0, (B) 1, (C) 2, and (D) 3. (E) Total RNA was isolated from each cell line and miR-342 expression levels analyzed by qRT-PCR were normalized to RNU44. [score:3]
Figure 4 Restored miR-342 expression sensitizes resistant cells to tamoxifen. [score:3]
Similar coordinate expression between EVL and miR-342 has been reported in colorectal cancer [24]. [score:3]
Our results indicate that miR-342 expression alone is not sufficient to induce cell death, but miR-342 sensitizes cells to apoptosis associated with estrogen-deprivation and tamoxifen exposure. [score:3]
Consistent with a role for miR-342 in tamoxifen induced apoptosis, the "Cell Death" biological function and more specifically "Apoptosis of Breast Cancer Cells" was the biological function most significantly (p < 7 × 10 [-6]) enriched with miR-342 regulated genes. [score:2]
Although we failed to obtain significance due to the small number of tumor samples, we did find that responders had nearly two-fold the levels of miR-342 expression when compared to tumors from patients that failed tamoxifen therapy (1.5 +/- 0.3 vs. [score:2]
When canonical cellular pathways were analyzed for miR-342 regulated genes, IPA identified miR-342 genes most significantly enriched in the "Mitotic Roles of Polo-Like Kinase" pathway (p < 0.0001)(Figure 6A). [score:2]
Enhanced expression of miR-342 in tamoxifen sensitive breast tumor cells has been reported previously, however, the functional significance of deregulated miR-342 was not investigated by this group [13]. [score:2]
Consistent with these results, qRT-PCR analyses showed that miR-342 is suppressed in the tamoxifen resistant MCF-7/HER2Δ16 and TAMR1 cell lines when compared to tamoxifen sensitive MCF-7/pcDNA cells (Figure 1B). [score:2]
Ingenuity Pathways Analysis of the dataset revealed a significant influence of miR-342 on multiple tumor cell cycle regulators. [score:2]
Pathways most significantly enriched with miR-342 regulated genes included (A) Mitotic Roles of Polo-Like Kinase (p < 0.0001) and (B) Hereditary Breast Cancer Signaling (p < 0.002). [score:2]
Importantly, reintroduction of miR-342 sensitized refractory breast tumor cells to tamoxifen therapy suggesting that miR-342 is an important regulator of tamoxifen response. [score:2]
miR-342 Regulates Genes Associated with Tumor Cell Death and Cancer Pathways. [score:2]
Figure 6 Ingenuity Pathway Analysis (IPA) of miR-342 regulated genes. [score:2]
The next breast cancer relevant pathway significantly enriched with miR-342 regulated genes was "Hereditary Breast Cancer Signaling" (p < 0.002) which includes multiple genes with obvious connections to breast cancer (Figure 6B). [score:2]
Taken together our results provide a genomic basis to explore the role of miR-342 regulated genes in multiple tamoxifen actions including both apoptosis and cytostasis. [score:2]
In situ hybridization of miR-342 In situ hybridization (ISH) of 6 μm sections from archived FFPE primary breast tumor specimens was performed using standard techniques and double-DIG Locked Nucleic Acid -modified DNA probe complementary to mature hsa-miR-342-3p or scrambled control (Exiqon) according to the manufacturer's instructions. [score:1]
In situ hybridization of miR-342. [score:1]
We focused follow-up analysis on miR-342-3p (miR-342) which was the most dramatically altered miRNA in the tamoxifen resistant MCF-7/HER2Δ16 cells and miR-342 has recently been shown to be associated with ERα(+) and HER2 (+) breast tumors [23]. [score:1]
Membranes were then hybridized (42°C for 16 h) with P [32]-labeled DNA probes corresponding to the complementary sequences of the mature miR-342-3p. [score:1]
DMC performed all miR-342 and apoptosis analyses as well as prepared the manuscript draft. [score:1]
Similar to our findings that miR-342 sensitizes breast tumor cells to tamoxifen, TXNIP sensitizes breast tumor cells to paclitaxel [38]. [score:1]
PMD performed all miR-342 and cell growth analyses required for the revised manuscript. [score:1]
RNA was analyzed by Northern Blot using DNA probes specific for miR-342-3p (miR-342) and the 5S RNA loading control. [score:1]
In situ hybridization (ISH) of 6 μm sections from archived FFPE primary breast tumor specimens was performed using standard techniques and double-DIG Locked Nucleic Acid -modified DNA probe complementary to mature hsa-miR-342-3p or scrambled control (Exiqon) according to the manufacturer's instructions. [score:1]
Quantification of miR-342. [score:1]
Pre-miR miRNA Precursor Molecules (Ambion) for hsa-miR-342-3p were transfected into cell lines at the indicated concentrations using Hyperfect (Qiagen). [score:1]
NSS and SME performed miR-342 ISH experiments. [score:1]
In summary, we have identified miR-342 as an important mediator of tamoxifen response in both breast tumor cell lines and breast cancer patients. [score:1]
We are currently investigating a similar mechanism of miR-342 suppression in tamoxifen resistant breast tumor cells. [score:1]
We propose that miR-342 may emerge as an important marker for tamoxifen response as well as a potential therapeutic. [score:1]
Either pCMV-miR-342 or pCMV-puro-NC were transfected into MCF-7/HER2Δ16 cells using Fugene6 (Roche) and stable clones were isolated. [score:1]
Nevertheless, activity of miR-342 appears to be functionally different in colorectal and breast tumor cells. [score:1]
Total RNA from biological triplicates of MCF-7/HER2Δ16-miR-342 and MCF-7/HER2Δ16-puro-NC was labeled and hybridized to Affymetrix GeneChip Human Exon 1.0 ST Array and data was analyzed using GeneSpring GX 9.0 (Agilent) software at the University of Colorado Denver DNA Microarray Core Facility. [score:1]
MCF-7 cells were plated at 5000 cells per well in a 48 well plate and transfected with 20 nM of hsa-miR-342-3p (Ambion) or pre-miR negative control (Ambion) using Hyperfect. [score:1]
The tamoxifen sensitive MCF-7/pcDNA and MCF-7/HER2 cell lines cultured for 48 hr in 5% CS-FBS MEM were transfected with anti-miR-342 or anti-miR negative control (NC) and the next day treated with 100 pM E2 alone or in combination with 1.0 μM TAM for five days. [score:1]
Despite the efforts of several laboratories, the physiological targets for miR-342 remain uncharacterized. [score:1]
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[+] score: 304
The resulting predicted miR-342-3p targets showed the best correlation with miR-342-3p -dependent repression of gene expression in our experimental system (Fig.   6d); 813 predicted miR-342-3p target genes were downregulated in pre-miR-342-3p -transfected cells (Fig.   6a; Additional file 11). [score:10]
a Relative expression heatmap of selected potential anti-apoptotic miR-342-3p target gene expression in miR -negative control (miR-neg) and miR-342-3p -overexpressing RAW264.7 cells 18 h after miRNA mimic transfection in three independent experiments (significance of repression is indicated after the gene name: *FDR ≤0.1, **FDR ≤0.05, ***FDR ≤0.01). [score:9]
Microarray analysis of miR-342-3p and miR -negative control -transfected cells identified 2640 downregulated and 2341 upregulated genes (FDR <0.1) in miR-342-3p -overexpressing macrophages compared with negative control -transfected cells (Fig.   6a; Additional file 10). [score:8]
The IL-4 -induced upregulation of miR-342-3p and downregulation of miR-99b and miR-125a-5p proved to be STAT6 -dependent, which was also validated by stem-loop RT-qPCR (Fig.   3c). [score:7]
The IL-4-regulated expression of miR-342-3p, miR-99b, and miR-125a-5p is dependent on IL-4Rα and STAT6 expression as demonstrated by loss of function genetic experiments. [score:6]
In silico target prediction and functional analyses identified the anti-apoptotic direct target gene network of miR-342-3p, which includes Bcl2l1. [score:6]
The 3′ UTR sequences corresponding to selected downregulated and computationally predicted anti-apoptotic mmu-miR-342-3p target genes were obtained using the TxDb. [score:6]
Set size and the statistical significance of each set being more repressed than genes with no potential target site are shown in parentheses Our transcriptome analysis revealed cellular proliferation and cell death as major target processes regulated by miR-342-3p. [score:6]
These findings raise the possibility that these downregulated genes are repressed directly by miR-342-3p. [score:5]
In silico analysis using the TargetScan target prediction algorithm showed two predicted mir-342-3p binding sites within the 3′ UTR of Bcl2l1 (Fig.   8c, miR-342-3p_I and miR-342-3p_II) [74]. [score:5]
The expression of miR-342-3p was unchanged while miR-193b expression was slightly induced during the monocyte-to-macrophage transition, while both increased significantly in response to IL-4. In contrast, miR-99b and miR-125a-5p showed a significant induction during monocyte–macrophage differentiation. [score:5]
Taken together, the combination of our in silico and experimental approaches suggest the miR-342-3p -dependent repression of Bcl2l1 expression, however, the demonstration of direct regulation requires further analysis. [score:5]
The combination of gene expression studies and chromatin immunoprecipitation experiments demonstrated that both miR-342-3p and its host gene, EVL, are coregulated directly by STAT6. [score:5]
In line with our in vitro results, miR-342-3p expression was upregulated in nematode-elicited macrophages 3 days after B. malayi implantation compared with naïve cells and showed continuously decreasing kinetics at later time points (Fig.   2b). [score:5]
In addition, Sylamer analysis of the microarrays derived from miR-342-3p and miR -negative control -transfected cells showed that the complementary sequence of the 8-mer seed region of miR-342-3p was enriched within the 3′ UTR of downregulated genes in miR-342-3p -transfected cells, confirming the specificity of the miR-342-3p -induced transcriptomic changes (Fig.   6c). [score:4]
Accordingly, we found that IL-4 induces Stat6 binding of an adjacent genomic region of Evl in mouse and human macrophages (+4 kb and −4 kb in mouse; +0.3 kb in human), suggesting that Evl and miR-342 are direct targets of IL-4/Stat6 signaling in both human and murine alternative macrophage activation. [score:4]
miR-342-3p is encoded within the third intron of the EVL gene in humans and mice and its expression showed coordinated regulation in both human colorectal cancer and multiple myeloma [63, 64]. [score:4]
Furthermore miR-342-3p has been described to be aberrantly downregulated in different malignancies, including colorectal and breast cancers [58, 63]. [score:4]
We studied the regulation of miR-342-3p, miR-99b, and miR-125a-5p expression during IL-4 -induced differentiation in vitro in human and murine macrophages as well as in nematode implantation -induced alternatively activated murine macrophages in vivo. [score:4]
We found that increased miR-342-3p expression paralleled macrophage proliferation changes observed at the early stage of B. malayi -induced alternative macrophage activation, which suggests a potential role of miR-342-3p in regulating the amount of local viable macrophages [19]. [score:4]
Therefore, we focused our efforts on the identification of the upstream regulator(s) of miR-342-3p, miR-125a, and miR-99b expression during mouse alternative macrophage activation. [score:4]
Conserved IL-4Rα/STAT6 signaling -dependent regulation of miR-342-3p, miR-99b, and miR-125a-5p expression during in vitro and in vivo mouse alternative macrophage activation. [score:4]
In order to gain insights into the molecular pathways controlled by miR-342-3p, we examined the transcriptome of miR-342-3p -transfected RAW264.7 macrophages and identified a set of repressed miR-342-3p direct target genes using computational and biochemical approaches (a flowchart of experimental approaches is shown in Fig.   6a). [score:4]
Fig. 4Mechanism of IL-4 -dependent co-regulation of miR-342-3p and EVL expression in human and mouse macrophages. [score:4]
These results suggest that the conserved IL-4 -dependent regulation of miR-342-3p, miR-99b, and miR-125a-5p expression holds in vivo relevance. [score:4]
Thus, we hypothesized that IL-4 -induced miR-342-3p expression could be a potential negative feedback mechanism controlling excessive macrophage expansion upon Th2-type cytokine stimulus. [score:3]
We found that the significantly overrepresented miR-342-3p-regulated Gene Ontology (GO) categories included cellular metabolism and regulation of viable cell number, including cell proliferation and cell death (Fig.   6b). [score:3]
It would be interesting to examine if in vivo overexpression of pro-apoptotic miR-342-3p has therapeutic relevance in alternative macrophage activation -associated human diseases, including fibrosis and certain malignant tumors that are characterized by pathologic macrophage abundance. [score:3]
In contrast, the luciferase activity of the construct containing the miR-342-3p_II binding site was not affected significantly by miR-342-3p overexpression. [score:3]
These findings suggest that enhanced miR-342-3p expression is a component of a negative feedback loop controlling excessive macrophage proliferation during Th2-type inflammatory responses. [score:3]
However, miR-342-3p overexpression significantly increased the number of both AV -positive/PI -negative early (Fig.   7e, lower right quadrants) and AV/PI double positive late (Fig.   7e, upper right quadrants) apoptotic cells (Fig.   7e, f). [score:3]
Fig. 6Global transcriptome and in silico analysis -based miR-342-3p target gene identification. [score:3]
To identify those biological functions whose activity might be regulated by miR-342-3p, we analyzed the list of the most significantly regulated genes (FDR ≤0.01) using the ClueGO Cytoscape plugin [72]. [score:3]
In addition, we determined that both miR-342-3p and its host gene, EVL, are co-regulated directly by STAT6 in mouse and human macrophages. [score:3]
As expected, we found that both the IL-4 -mediated induction of miR-342-3p as well as the reduction of miR-99b and miR-125a-5p expression were completely abolished in IL-4Rα -deficient macrophages, confirming the requirement of the receptor for transmitting the IL-4 stimulus (Fig.   3a). [score:3]
Both Evl and miR-342-3p expression levels were induced during mouse BMDM differentiation, which was further increased by IL-4 in a STAT6 -dependent manner (Fig.   4b, c). [score:3]
We identified a miR-342-3p-repressed anti-apoptotic gene network with well characterized inhibitors of apoptosis, including Bcl2l1, Xiap, Api5, and Birc6 in macrophages by applying a combination of in silico target prediction algorithms and miRNA mimic experiments. [score:3]
These results thus raise the possibility of a connection between macrophage apoptosis and elevated miR-342-3p expression induced by Th2-type inflammation. [score:3]
We examined miR-193b and miR-342-3p as two of the highly expressed IL-4 -induced miRNAs. [score:3]
Indeed, our functional studies showed that miR-342-3p over -expression reduced viable macrophage number via induction of apoptosis. [score:3]
The comparison was used to verify direct effects due to miR-342-3p regulation. [score:3]
Interestingly, elevated expression of miR-342-5p (derived from the 5′ strand of the pre-miR-342 miRNA precursor) in inflammatory macrophages has been linked to the formation of atherosclerotic lesions [86]. [score:3]
Finally, we found that miR-342-3p is capable of controlling macrophage survival through targeting an anti-apoptotic gene network including Bcl2l1. [score:3]
We cotransfected the generated luciferase expression constructs with miR-342-3p and miRNA -negative control mimics into HEK293T cells. [score:3]
As shown in Fig.   7d, analysis of cell cycle distribution by Hoechst staining and slide -based imaging cytometry revealed that miR-342-3p overexpression was associated with a slight but not significant increase in the number of cells in S phase. [score:3]
To explore the direct miRNA–mRNA interactions, we selected Bcl2l1 as one of the central components of the miR-342-3p-regulated anti-apoptotic gene network for further analysis. [score:3]
c Stem-loop RT-qPCR -based quantification of miR-342-3p, miR-99b, and miR-125a-5p expression in IL-4-stimulated or unstimulated WT and Stat6 KO mouse bone marrow-derived macrophages. [score:3]
Based on this, we determined miR-342-3p, miR-99b, and miR-125a-5p expression in nematode-elicited macrophages at different time points after infection (the experimental design is shown in Additional file 3c). [score:3]
These findings suggest that miR-342-3p and its host gene, EVL, are coordinately regulated by IL-4 via direct DNA binding of STAT6 in both mouse and human macrophages. [score:3]
d Cumulative distributions of relative change (t-statistic) for different sets of potential miR-342-3p target genes with 7mer. [score:3]
a Schematic representation of combined microarray -based and computational miR-342-3p target gene identification. [score:3]
In addition, overexpression of miR-342-3p was found to induce apoptosis and block cancer cell proliferation [59, 63]. [score:3]
b Network visualization of Gene Ontology enrichment analysis of genes differentially expressed in miR-342-3p -transfected RAW264.7 mouse macrophages (FDR ≤0.01) using the ClueGO Cytoscape plugin. [score:3]
We generated luciferase expression constructs with the predicted miR-342-3p-containing 3′ UTR regions of Bcl2l1 or mutated versions (Fig.   8c). [score:3]
c Luciferase activity in HEK293T cells cotransfected with luciferase expression constructs containing WT or mutated (Del) miR-342-3p binding sites of Bcl2l1 and miR-342-3p/miRNA negative-control mimics (n = 6). [score:3]
c Sylamer analysis revealed that only miR-342-3p 8-mer seed matches were enriched among downregulated genes in miR-342-3p -transfected macrophages compared with miR -negative control -treated cells. [score:3]
miR-342-3p followed similar but delayed kinetics upon IL-4 treatment as its elevated expression was only detectable after 24 h (Fig.   4f; Additional file 6c). [score:3]
Intriguingly, elevated expression of miR-342-3p in the liver is accompanied by enhanced macrophage apoptosis in malaria-infected mice [93, 94]. [score:3]
Fig. 7Reduced cell viability and increased macrophage apoptosis by miR-342-3p overexpression. [score:3]
f Stem-loop RT-qPCR -based quantification of miR-342-3p expression during human macrophage differentiation in the absence or presence of IL-4 (a representative example of three independent human donors is shown). [score:3]
The cell number of miR-342-3p -overexpressing macrophages showed 40 and more than 80 % reduction at 24 and 48 h post-transfection, respectively, compared with the miR -negative control -transfected cells (Fig.   7a). [score:2]
Direct Stat6 -dependent induction of miR-342-3p and its host gene, EVL, during alternative activation of murine and human macrophages. [score:2]
Intriguingly, IL-4 -dependent regulation of miR-342-3p, miR-99b, and miR-125a-5p is conserved between human cells and mouse bone marrow-derived macrophages. [score:2]
miR-342-3p regulates cell proliferation and apoptosis -associated signaling pathways at the post-transcriptional level in macrophages. [score:2]
We observed that the majority of IL-4-regulated miRNAs were strictly STAT6 -dependent in mouse macrophages, including miR-342-3p, miR-125a-5p, and miR-99b-5p, as well as the previously studied miR-511-5p and miR-324-5p. [score:2]
The other selected IL-4-enhanced miRNA, mir-342-3p, is associated with pro-apoptotic and anti-proliferative functions in different tumor types; it may, therefore, be a potential negative feedback regulator of IL-4 -induced macrophage proliferation [11, 27, 58, 59]. [score:2]
We found that three IL-4-responsive miRNAs (miR-342-3p, miR-125a, and miR-99b) showed conserved regulation in both human and mouse alternatively activated macrophages in vitro and in B. malayi nematode-infected mice in vivo. [score:2]
These results are consistent with the notion that IL-4/STAT6 signaling -induced miR-342-3p is a potent negative feedback regulator of macrophage cell number via induction of apoptosis. [score:2]
However, further experimental confirmation is required for the demonstration of direct miR-342-3p -dependent repression. [score:2]
In addition, we found that Bcl2l1 is directly repressed by miR-342-3p. [score:2]
F1/R2 and F2/R1 as well as F3/R4 and F4/R3 primers were used to delete the mir-342-3p target sites from the 3′ UTR. [score:2]
Additionally, miR-342-3p and its host gene, Evl (Ena/Vasp-like), are co-regulated during IL-4 -induced alternative macrophage activation in mouse. [score:2]
As shown in Fig.   2a, miR-342-3p, miR-99b, and miR-125a-5p were regulated by IL-4 similar to the human cells. [score:2]
These findings strongly suggest a role for IL-4 -induced miR-342-3p as a potent negative feedback regulator of macrophage cell number via induction of apoptosis. [score:2]
In order to determine whether IL-4 -mediated co-regulation of EVL and miR-342-3p is conserved between human and mouse, we measured their expression in human monocyte-derived unstimulated and IL-4-stimulated macrophages. [score:2]
By using IL4Rα- and STAT6 -deficient macrophages, we were able to show that IL-4 -dependent regulation of miR-342-3p, miR-99b, and miR-125a-5p is mediated by the IL-4Rα–STAT6 signaling pathway. [score:2]
To further explore the IL-4 -dependent regulation of miR-342-3p and Evl in mice, we measured the expression of both mature miRNA and its host gene in mouse bone marrow cells as well as in IL-4-stimulated and unstimulated BMDMs. [score:2]
These findings suggest that the IL-4 -mediated regulation of miR-342-3p, miR-99b, and miR-125a-5p is conserved between humans and mice. [score:2]
From these results we concluded that miR-342-3p regulates macrophage cell numbers via induction of apoptosis. [score:2]
miR-342-3p acts as a regulator of macrophage cell number via reduction of cell viability and induction of apoptosis. [score:2]
IL-4 -dependent induction of miR-342-3p and repression of miR-99b along with miR-125a-5p occurred in both human and murine macrophages in vitro. [score:1]
Interestingly, the H3K4m3 peak was not detected in the intronic region of Evl around the miR-342-3p coding region, suggesting that Evl and miR-342-3p utilized a common TSS in resting and alternatively activated mouse macrophages (Fig.   4a). [score:1]
b Stem-loop RT-qPCR -based quantification of miR-342-3p, miR-99b, and miR-125a-5p in mouse thioglycolate-elicited and in vivo alternatively activated macrophages. [score:1]
First, we detected no activity of the miR-342-3p mimic on the 3′ UTR of Ago2, which does not contain a miR-342-3p binding site. [score:1]
In order to test this hypothesis, we sought to explore the functional effect of miR-342-3p on macrophage proliferation and/or apoptosis in the mouse macrophage cell line RAW264.7 transfected with miR-342-3p or miR -negative control miRNA mimics. [score:1]
c Stem-loop RT-qPCR -based measurement of miR-342-3p, miR-193b, miR-99b, and miR-125a-5p expression in human monocytes, 72-h nontreated, and IL-4-stimulated macrophages. [score:1]
After mixing the two PCR products and digestion with XhoI and NotI, the 3′ UTR fragment with deleted mir-342-3p binding sites was cloned into a XhoI/NotI-digested psiCHECK2 vector. [score:1]
miR-342-3p and murine miRNA seed matches are represented as red dashed lines and gray lines, respectively. [score:1]
Transfection was performed using PEI with 0.1 μg of pRL-TK (Rr-luc) containing 3′ UTR sequences and 0.1 μg of pGL3 control vector (Pp-luc) (Promega) for either a specific miR-342 or small interfering RNA control. [score:1]
b GeneMANIA -based identification of the miR-342-3p-repressed, anti-apoptotic gene network. [score:1]
Functional analyses combined with miRNA manipulation studies demonstrated that miR-342-3p decreases the viability of macrophages by inducing apoptosis. [score:1]
f Viable (PI-, AV-), early apoptotic (PI-, AV+) and late apoptotic (PI+, AV+) cell distribution 48 h following miR -negative control and miR-342-3p mimic transfection into RAW264.7 cells. [score:1]
Some miRNAs from our study, including miR-342-3p and miR-193b, may be promising candidates as potential biomarkers in combination with other well characterized alternative macrophage activation-specific genes and proteins in human diseases. [score:1]
We used GeneMANIA to investigate the potential interactions between the miR-342-3p-repressed anti-apoptotic genes and found that 19 out of 23 predicted miR-342-3p target genes formed an anti-apoptotic gene network showing extensive predicted interactions and colocalization [73] (Fig.   8b). [score:1]
Seven cells at different time points following miR-342-3p mimic transfection. [score:1]
a Stem-loop RT-qPCR -based measurement of miR-342-3p, miR-193b, miR-99b, and miR-125a-5p expression in IL-4-stimulated and unstimulated mouse bone marrow-derived macrophages. [score:1]
Finally, we demonstrated that macrophage survival was reduced via miR-342-3p -dependent repression of an anti-apoptotic gene network. [score:1]
The mutated constructs contained a nine-nucleotide deletion of miR-342-3p binding regions. [score:1]
PsiCHECK2 dual luciferase vector (Promega) was used to confirm the function of the putative miR-342-3p binding sites in the Bcl2l1 3′ UTR. [score:1]
Moreover, our study indicates that miR-342-3p likely plays a pro-apoptotic role in such cells, thereby providing a negative feedback arm to IL-4 -dependent macrophage proliferation. [score:1]
The comparison used was transfection with miR-342-3p versus miR -negative control miRNA mimics in the mouse macrophage cell line RAW264.7. [score:1]
miR-342-3p mimic -dependent reduction of luciferase activity was completely abolished when the miR-342-3p_I binding site was deleted (Fig.   8c). [score:1]
For luciferase reporter assays, 320 bp (miR-342-3p_1) and 309 bp (miR-342-3p_2) of the 3′ UTR of the Bcl2l1 gene, including the mir-342-3p target sites, were amplified by PCR using F1/R1 and F3/R3 primer pairs with XhoI and NotI sites. [score:1]
miR-342-3p also has pro-apoptotic and anti-proliferative roles in colorectal and breast cancer cells [58, 59, 63]. [score:1]
We found IL-4 -dependent induction of miR-342-3p and miR-193b and repression of miR-99b and miR-125a-5p. [score:1]
a miR-342-3p, miR-99b, and miR-125a-5p expression in IL-4-stimulated or unstimulated wild-type (WT) and IL-4Rα-defficient (IL-4Rα KO) mouse bone marrow-derived macrophages as measured by stem-loop RT-qPCR. [score:1]
These are the likely enhancers controlling Evl as well as miR-342-3p induction. [score:1]
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[+] score: 250
In consistent with in vitro results, knockdown of H19 markedly decreased the protein expression level of FOXM1, and inhibiting miR-342-3p significantly up-regulated FOXM1 expression (Fig.   7c). [score:11]
Compared to the control group, the RNA and protein levels of FOXM1 were down-regulated after H19 silencing in NOZ and GBC-SD cells and up-regulated by transfecting with miR-342-3p inhibitors; but in the group of co-transfecting with miR-342-3p inhibitor and siRNA-H19, the modulating effects of H19 on FOXM1 were diminished (Fig.   3a– d). [score:10]
QRT-PCR and assays demonstrated that H19 silencing down-regulated, whereas over -expression enhanced the expression of miR-342-3p targeting FOXM1 through competitively ‘sponging’ miR-342-3p. [score:9]
In addition, we found that miR-342-3p targeted FOXM1 and negatively regulated FOXM1 expression, indicating that H19 could influence the expression of FOXM1 in GBC through miR-342-3p (Fig.   8). [score:8]
NOZ cells (1× 10 [6]) stably expressing control shRNA or H19 shRNA, or miR-342-3p inhibitor (an anti-miR-342-3p Oligonucleotides, purchased from Hanbio, Shanghai, China) or H19 shRNA + miRNA-342-3p inhibitor were subcutaneously injected into either side of flank area of 3-week-old Male nude mice (n = 4 mice per group). [score:7]
Fig. 7H19 oncogenic activity is in part through negative regulation of miR-342-3p in vivo (a) Representation picture of tumor formation of xonograft in nude mice in lv-control, lv-shRNA-H19, lv-miR-342-3p inhibitor and lv-shRNA-H19+ miR-342-3p inhibitor group, respectively (each group n = 4). [score:6]
The expression of H19 was not changed by miR-342-3p mimic or miR-342-3p inhibitor, which indicated that H19 was the upstream of miR-342-3p. [score:5]
We next verified whether H19 modulated the expression of FOXM1 by targeting miR-342-3p in GBC cells. [score:5]
f The expression of miR-342-3p after over -expression of H19 was detected by qRT-PCR in GBC-SD cells (P < 0.05). [score:5]
MiR-342-3p mimic or negative control mimic and has-miR-342-3p inhibitor or negative control inhibitor were purchased from Genepharma, Shanghai, China. [score:5]
On the contrary, miR-342-3p expression was decreased significantly after over -expression of H19 in GBC-SD cells (P < 0.05) (Fig.   1c and f). [score:5]
a- b Cell invasion ability and invasive cells number were detected by transfecting si-NC, siH19, miR-342-3p inhibitor, and siH19+ miR-342-3p inhibitor into NOZ cells (P < 0.05). [score:5]
g The expression of H19 after transfected of miR-342-3p inhibitor or mimic. [score:5]
Fig. 3H19 modulated expression of endogenous miR-342-3p targeting FOXM1. [score:5]
However, the exogenous miR-342-3p inhibitors or mimics did not alter the expression of H19 (Fig.   1g). [score:5]
c Representation of FOXM1 expression in xenografts tumor using IHC method in lv-control, lv-shRNA-H19, lv-miR-342-3p inhibitor and lv-shRNA-H19+ miR-342-3p inhbitor group, respectively. [score:5]
H19 modulated expression of endogenous miR-342-3p targets FOXM1. [score:5]
Our results suggest a potential ceRNA regulatory network involving H19 regulates FOXM1 expression by competitively binding endogenous miR-342-3p in GBC. [score:5]
c- d Cell invasion ability and invasive cells number were detected by transfecting si-NC, siH19, miR-342-3p inhibitor, and siH19+ miR-342-3p inhibitor into GBC-SD cells (P < 0.05). [score:5]
a- b The mRNA levels and protein levels of FOXM1 in NOZ cells transfected with si-NC, si-H19, miR-342-3p inhibitor, and si-H19 + miR-342-3p inhibitor. [score:5]
c- d Cell cycle was detected by transfecting si-NC, siH19, miR-342-3p inhibitor and siH19+ miR-342-3p inhibitor into GBC-SD cells (P < 0.05). [score:5]
a- b cell cycle were detected by transfecting si-NC, siH19, miR-342-3p inhibitor and siH19+ miR-342-3p inhibitor into NOZ cells (P < 0.05). [score:5]
c- d The mRNA levels and protein levels of FOXM1 in GBC-SD cells transfected with si-NC, si-H19, si-H19 + miR-342-3p inhibitor, and miR-342-3p inhibitor. [score:5]
In conclusion, we suggest a potential ceRNA regulatory network involving H19 and miR-342-3p in the modulation of FOXM1 expression. [score:4]
These results suggested that H19 directly targeted miR-342-3p. [score:4]
All data were represented as the mean ± S. D. from three independent experiments, ** P < 0.05 To explore whether miR-342-3p was targeted and directly bound to H19, fragments of wild-type and mutated H19 cDNA sequence containing the putative miR-342-3p recognition site (predicted in starbase 2.0) (Fig.   2c) was cloned. [score:4]
Furthermore, transwell invasion assays and cell cycle assays indicated that H19 knockdown inhibited both cells invasion and proliferation, but this effects was attenuated by co-transfection of siRNA-H19 and miR-342-3p inhibitor in GBC cells. [score:4]
Simultaneous knockdown of H19 and inhibited miR-342-3p had no impact on tumor formation (Fig.   7a and b). [score:4]
All data were represented as the mean ± S. D. from three independent experiments, ** P < 0.05To explore whether miR-342-3p was targeted and directly bound to H19, fragments of wild-type and mutated H19 cDNA sequence containing the putative miR-342-3p recognition site (predicted in starbase 2.0) (Fig.   2c) was cloned. [score:4]
We discovered that knocked down H19 in GBC cell lines increased the endogenous level of miR-342-3p (Fig.   1d, e), and these effects were neutralized by exogenous miR-342-3p inhibitor (Fig.   3a– d). [score:4]
b Summery of tumor volume of mice which were measured in every week in lv-control, lv-shRNA-H19, lv-miR-342-3p inhibitor and lv-shRNA-H19+ miR-342-3p inhibitor group, respectively. [score:3]
We showed that H19 probe harbored the Ago2 protein and detected the expression of miR-342-3p in the same pellet, the antisense strand of H19 probe was used as negative control (Fig. 2e and f). [score:3]
The expression of miR-342-3p was normalized to U6. [score:3]
Fig. 1Expression of H19 in GBC and its effect on miR-342-3p. [score:3]
d– e The expression level of miR-342-3p after H19 silencing in NOZ and EHGB-1 cells was detected by qRT-PCR (P < 0.05). [score:3]
Initially, compared to the control group, knockdown of H19 decreased the number of invasive cells in NOZ and GBC-SD cells, but was reversed by co-transfection of siRNA-H19 and miR-342-3p inhibitor simultaneously (Fig.   5a– d). [score:3]
FOXM1 was a well-accepted oncogene that is targeted by miR-342-3p in cervical cancer [35]. [score:3]
By dual-luciferase reporter assays, RNA -binding protein immunoprecipitation (RIP) ands, we verified that H19 was identified as a direct target of miR-342-3p. [score:3]
In this study, the expression of H19 and miR-342-3p were analyzed in 35 GBC tissues and matched normal tissues by using quantitative polymerase chain reaction (qRT-PCR). [score:3]
We demonstrated H19 was overexpressed and negatively correlated with miR-342-3p in GBC. [score:3]
Similarly, the RNA and protein levels of FOXM1 were both increased after cells transfected by overexpression H19 in GBC-SD, however, the effects were counteracting after co-transfection of H19 plasmids and miR-342-3p mimic (Fig.   3e and f). [score:3]
Interestingly, miR-342-3p exerted tumor suppression effects in GBC, which was consistent with other findings in lung cancer [45], hepatocellular carcinoma [46] and cervical cancer [35]. [score:3]
H19 negatively regulated miR-342-3p in GBC, through binding to miR-342-3p directly. [score:3]
Lv-miR-342-3p inhibitor significantly increased the oncogenic ability of NOZ cells. [score:3]
In addition, the expression level of H19 was significant negatively correlation with miR-342-3p (R = −0.403, P < 0.05) (Fig.   2b). [score:3]
b Pearson’s correlation was used for correlation analysis between the expression of H19 mRNA and miR-342-3p mRNA (R = −0.403, P < 0.05). [score:3]
In this study, we demonstrated that H19 modulated FOXM1 expression by competitively ‘sponging’ to miR-342-3p, which led to promote cells proliferation and invasion in GBC cells. [score:3]
a Expression level of miR-342-3p in pair samples of GBC and normal tissues was detected by qRT-PCR (n = 35, P < 0.05). [score:3]
In cell cycle assay in NOZ and GBC-SD cells, knockdown of H19 induced cell cycle arrest in G0/G1 phase, but was reversed by co-transfection of siRNA-H19 and miR-342-3p inhibitor (Fig.   6a– d). [score:3]
MiR-342-3p expression levels were markedly increased after silencing H19 in NOZ and EHGB-1 cells (P < 0.05) (Fig.   1d– e). [score:2]
In vivo, tumor volumes were decreased significantly in H19 silenced group compared to the control group, but was attenuated by co-transfection of shRNA-H19 and miR-342-3p inhibitor, which were stablely constructed through lenti-virus vector. [score:2]
H19 oncogenic activity is in part through negative regulation of miR-342-3p in vivo. [score:2]
Our results proposed that H19 functioned as a ceRNA for miR-342-3p, a new miRNA, to regulate FOXM1 epigenetically. [score:2]
The potential mechanism of the negative regulation of miR-342-3p by H19. [score:2]
To uncover the mechanism of H19 regulation in GBC, we discovered that H19 shared miR-342-3p response element with FOXM1, an important oncogene that has been reported to be associated with many cancers [42– 44]. [score:2]
Fig. 5H19/miR-342-3p/FOXM1 axis on cell invasion in GBC cells. [score:1]
Furthermore, the results of dual-luciferase reporter assay, RNA -binding protein immunoprecipitation assay and indicated that H19 was a target of miR-342-3p. [score:1]
All data were represented as the mean ± S. D. from three independent experiments, ** P < 0.05 We continued to explore the effects of H19/miR-342-3p/FOXM1 axis on invasion and cell cycle in GBC cells. [score:1]
Four lenti-virus constructed cells including lv-control, lv-sh-H19, lv-miR-342-3p inh and lv-miR-342-3p inh + lv-sh-H19 were well cultured and were injected subcutaneously. [score:1]
c Representation the H19 and miR-342-3p binding site by miRanda (http://www. [score:1]
To determine whether H19 is associated with the RISC complex, we performed using biotin labeled H19 as a probe and then detected Ago2 from the pellet by western-blotting and miR-342-3p by qRT-PCR. [score:1]
H19 miR-342-3p Competing endogenous RNA FOXM1 Gallbladder cancer Gallbladder cancer (GBC) is the most common biliary tract cancer and the fifth most common gastrointestinal malignancy [1]. [score:1]
It is worth noting that the relationship between H19 and FOXM1 depends on miR-342-3p. [score:1]
All data were represented as the mean ± S. D. from three independent experiments, ** P < 0.05 Fig. 6H19/miR-342-3p/FOXM1 axis on cell cycle in GBC cells. [score:1]
d Statistical analyses of IHC results in xenograft tumor in lv-control, lv-shRNA-H19, lv-miR-342-3p inhbitor and lv-shRNA-H19+ miR-342-3p inhbitor group, respectively To sum up, a ceRNA mo del was proposed to summarize H19/miR-342-3p/FOXM1 pathway (Fig.   8). [score:1]
We focused on miR-342-3p, which had the greatest fold-change. [score:1]
Two ng of pRL-TK (Promega, Madison, WI, USA) were also co -transfected with miR-342-3p mimic or miRNA NC into HEK293T cells by using Lipofectamie 2000 (Invitrogen, USA). [score:1]
d Luciferase activity in HEKT293 cells cotransfected with miR-342-3p mimic and luciferase reporters containing control vector, pmir-Glo-H19-wt and pmir-Glo-H19-mut (P < 0.05). [score:1]
d Statistical analyses of IHC results in xenograft tumor in lv-control, lv-shRNA-H19, lv-miR-342-3p inhbitor and lv-shRNA-H19+ miR-342-3p inhbitor group, respectivelyTo sum up, a ceRNA mo del was proposed to summarize H19/miR-342-3p/FOXM1 pathway (Fig.   8). [score:1]
H19/miR-342-3p/FOXM1 axis on cell invasion and cell cycle in GBC cells. [score:1]
These results indicated that miR-342-3p might have an interaction with H19. [score:1]
e- f The mRNA levels and protein levels of FOXM1 in GBC-SD cells transfected with pLv-CMV, miR-342-3p mimic, pLv-CMV-H19, miR-342-3p mimic + pLv-CMV-H19. [score:1]
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[+] score: 214
In the present study, miR-342 expression was shown to be positively correlated with the expression of ERα in human breast cancer tissues and the introduction of miR-342 into estrogen -dependent breast cancer cells was shown to upregulate ERα expression and enhance tamoxifen sensitivity with decreased cellular proliferation and increased apoptosis. [score:10]
The ectopic expression of miR-342 upregulated ERα mRNA levels and promoted tamoxifen sensitivity in MCF-7 cells, whereas the knockdown of miR-342 reduced ERα mRNA expression and weakened tamoxifen sensitivity. [score:9]
The results of the present study show that the expression levels of miR-342 were markedly higher in the ERα -positive breast cancer tumors than in the ERα -negative tumors and that the levels of miR-342 gradually increased as ERα mRNA expression increased, suggesting that miR-342 is a key factor for the regulation of ERα expression in the development and progression of human breast cancer. [score:9]
Quantitative RT-PCR detection analysis showed that the expression levels of miR-342 were markedly higher in the ERα -positive tumors (1.386±0.480) than in the ERα -negative tumors (0.785±0.315; P= 0.000), that the miR-342 expression levels were increased in the HER2 -negative tumors (1.416±0.432) compared with the HER2 -positive tumors (1.017±0.492; P= 0.001) and that miR-342 expression was upregulated in the VEGF -negative tumors (1.416±0.432) compared with the VEGF -positive tumors (1.088±0.528; P= 0.031). [score:8]
By contrast, inhibition of miR-342 in the MCF-7 cells downregulated the ERα expression and weakened the response to tamoxifen, with increased cellular proliferation and decreased apoptosis. [score:8]
The ERα mRNA expression was analyzed by RT-PCR, which showed that the levels of ERα mRNA expression were upregulated in the group transfected with the miR-342 mimics compared with those in the control group and decreased in the group transfected with the miR-342 inhibitors compared with those in the control group (Fig. 2C and D). [score:8]
By contrast, the suppression of miR-342 is able to inhibit cellular proliferation less following the transfection with miR-342 inhibitors than the cells with the NC (0.729±0.019 vs. [score:7]
The miR-342 expression was markedly lower when using the miR-342 inhibitors than when using the miR-342 inhibitor NCs (P=0.000; Fig. 2B). [score:7]
The study reported for the first time that the levels of miR-342 expression were positively correlated with ERα mRNA expression and also revealed a correlation between increased tamoxifen sensitivity and the elevated levels of ERα mRNA by augmenting the miR-342 expression. [score:7]
The results showed that 96 h after the use of miR-342 mimics or inhibition transfection, the overexpression or suppression of miR-342 was not able to change cellular proliferation. [score:7]
To analyze the association between the miR-342 expression and the ERα mRNA expression, the expression levels were plotted. [score:7]
As miR-342 is not differently expressed between the breast cancer and cancer adjacent tissues, we forecast that miR-342 would not play a tumor-suppressive or tumor-promotive role in breast cancer development. [score:6]
For this purpose, miR-342 -overexpressing or miR-342-suppressing MCF-7 cells were treated with 15 μM tamoxifen for 48 h, then cell apoptosis was analyzed with flow cytometry under the same conditions. [score:5]
miR-342 expression is positively correlated with ERα mRNA expression in human breast cancer and cell lines. [score:5]
Based on these observations, we propose that the levels of miR-342 expression that correspond to the ERα mRNA expression locus may act as a biomarker for tamoxifen sensitivity in ERα -positive breast cancer. [score:5]
The scatterplots showed that miR-342 expression was positively correlated with ERα mRNA expression in human breast cancer (P=0.003; Fig. 1F). [score:5]
In conclusion, the present data indicated for the first time that miR-342 expression is positively correlated with the expression of ERα mRNA in human breast cancer tissues and that the introduction of miR-342 into estrogen -dependent breast cancer cells enhances tamoxifen sensitivity. [score:5]
However, in the presence of 20 μM tamoxifen for 72 h, ectopic miR-342 expression was able to suppress cellular proliferation to a greater extent following transfection with the miR-342 mimics than the cells transfected with the NC (0.459±0.013 vs. [score:5]
The results of the present study indicated that miR-342 expression alone was not sufficient to induce cell death, but that miR-342 sensitizes cells to cellular proliferation inhibition and apoptosis associated with tamoxifen exposure. [score:5]
For the first time miR-342 expression was identified as positively correlated with ERα mRNA expression. [score:5]
It has been shown that the downregulation of miR-342 is associated with ERα -negative breast cancer (8) and tamoxifen-resistant breast tumors (16). [score:4]
Cittelly et al(16) reported that there was no evident association between the direct targets of miR-342 and the tumor cell response to tamoxifen. [score:4]
The present study was undertaken to assess the expression of miR-342 and ERα mRNA in human breast cancer samples. [score:3]
Correlations between the expression levels of miR-342 and the clinicopathological factors. [score:3]
The present study demonstrated that the expression of miR-342 in the ERα -positive breast cancer tumors and cells was significantly greater than that in the ERα -negative breast cancer tumors and cells. [score:3]
These results indicated that miR-342 may emerge as a significant marker for the tamoxifen response, as well as as a potential therapeutic target. [score:3]
Conversely, the apoptotic percentage was lower in the miR-342-suppressing MCF-7 cells than in the NC (3.06±0.42 vs. [score:3]
Cittelly et al(16) demonstrated that miR-342 was markedly suppressed in multiple tamoxifen-resistant breast tumor cell lines and in primary breast tumors of patients whose tamoxifen therapy failed. [score:3]
The results showed that the apoptotic percentage was higher in the miR-342 -overexpressing cells than in the NC (9.54±1.14 vs. [score:3]
Next the ERα mRNA and miR-342 expression levels were examined in the human breast cancer tissues. [score:3]
In addition, the results showed that the levels of miR-342 expression increased in VEGF -negative, HER2 -negative and Luminal-A breast cancer samples. [score:3]
This result is consistent with the observations of the present study that showed that ectopic miR-342 expression sensitized MCF-7 cells to tamoxifen -induced apoptosis. [score:3]
Similarly, miR-342 expression in colorectal cancer cells results in tumor cell apoptosis (20). [score:3]
The miR-342-3p mimics, miR-342-3p inhibitor and the negative control (NC) were purchased from Jima Co. [score:3]
Correlations between the expression levels of miR-342 and clinicopathological factors were analyzed. [score:3]
No discrepancy exists in the miR-342 expression between the cancer (1.404±0.529) and cancer adjacent (1.151±0.387; P=0.065) in this study. [score:3]
There was no evident relevance between the levels of miR-342 expression and PR, lymph node metastasis status or the pathological grade (P>0.05; Table I). [score:3]
miR-342 elevates ERα mRNA expression of MCF-7 cells and promotes tamoxifen sensitivity. [score:3]
The expression levels of miR-342 in the 48 human breast cancer tissues were examined. [score:3]
The MCF-7 cells were transfected with the miR-342 mimics at a concentration of 10 nM or with the miR-342 inhibitors at a concentration of 20 nM. [score:3]
The control groups were transfected with the miR-342 NCs or with the miR-342 inhibitor NCs. [score:3]
First the expression levels of ERα mRNA and miR-342 were assessed in the breast cancer cell lines and the results showed that they were greatly increased in the ERα -positive cells (MCF-7) compared with those in the ERα -negative cells (SKBR-3 and MB-231; P<0.05; Fig. 1A–C). [score:2]
Significantly, the reintroduction of miR-342 sensitized the refractory breast tumor cells to tamoxifen therapy, suggesting that miR-342 is a significant regulator of the tamoxifen response. [score:2]
Ingenuity Pathway Analysis of the entire set of genes significantly altered by miR-342 revealed a significant association between the miR-342-regulated genes and cell apoptosis. [score:2]
The results showed that the miR-342 expression was significantly increased in the MCF-7 cells following transfection with the miR-342 mimics, when compared with control group treated with the mimic NCs (P=0.000; Fig. 2A). [score:2]
Transfection with the miR-342 inhibitors compared with the NC, (2.363±0.1999 vs. [score:2]
This series of analyses demonstrated that the miR-342 indeed plays a key role in changing the response of MCF-7 cells to tamoxifen. [score:1]
As the VEGF -negative, HER2 -negative and Luminal-A signals indicate a good prognosis, miR-342 may be a biomarker of predicting a good prognosis for breast cancer. [score:1]
As tamoxifen is known to induce apoptosis in breast cancer cells (18), the potential role of miR-342 in promoting tamoxifen -mediated apoptosis was explored. [score:1]
miR-342 may be a novel candidate for ERα-specific endocrine therapy in breast cancer. [score:1]
Nevertheless, the activity of miR-342 appears to differ functionally in colorectal and breast tumor cells. [score:1]
Previous studies have shown that miR-342 is an ERα -associated miRNA (8). [score:1]
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5
[+] score: 117
In the present study, we also showed that overexpression of the miR-342, which targets the 3′-UTR (untranslated region) of IA-2, results in a decrease in the expression of IA-2 mRNA and, in turn, a decrease in the cellular content and secretion of ACh resulting in a decrease in the growth of SCLC cells (Fig.   6). [score:9]
As seen in Fig.   3, the miR-342 mimic significantly decreased the expression of IA-2 mRNA, whereas the miR-342 inhibitor significantly enhanced the expression of IA-2 mRNA in both cell lines (Fig.   3a, b). [score:7]
Recently, we found that IA-2 is a target of the microRNA miR-342 and that miR-342 mimics suppress the expression of IA-2. The present experiments were initiated to see whether IA-2 and/or miR-342 affect the growth of SCLC. [score:7]
Western blot analysis showed that miR-342 mimic decreased, whereas miR-342 inhibitor enhanced protein expression in both cell lines (Fig.   3c–f). [score:5]
a, b Effects of miR-342 mimic and miR-342 inhibitor on IA-2 expression in NCI-H82 and NCI-H345 cells (n = 4), as quantitated by Real-Time PCR. [score:5]
miR-342 regulates IA-2 expression in SCLC cells. [score:4]
MiR-342 mimic suppresses IA-2 expression, SCLC cell growth and ACh content and secretion. [score:4]
e, f Relative expression levels of IA-2 in Western blots (normalized by α-tubulin), were determined by NIH Image J. *p < 0.05; **p < 0.01 Given that miR-342 directly targets IA-2 as previously demonstrated in the insulin-containing MIN6 cells by “RNA immunoprecipitation PCR with anti-argonaute 2” [25], the impact of miR-342 on SCLC cell proliferation was evaluated. [score:4]
In this context, a recent microarray analysis showed that miR-342 is one of the most downregulated miRNAs associated with lung cancer [23]. [score:4]
Taken together, the demonstration that both miR-342 and its target gene IA-2 are involved in the growth of SCLC cells, through their effect on the secretion of acetylcholine, represents a novel approach that may be therapeutically useful in the treatment of SCLC tumors. [score:3]
ACh rescues the inhibitory effects IA-2 siRNA or miR-342 mimic on SCLC proliferation. [score:3]
A barely significant increase in cell growth was observed in the cells treated with the miR-342 inhibitor (96 h after treatment; n = 6). [score:3]
Fig.  4Inhibitory effect of miR-342 mimic on SCLC growth and ACh secretion. [score:3]
NCI-H82 cells treated with the miR-342 inhibitor showed a slight but not significant increase in ACh secretion (Fig.   4e–f), and a barely significant increase in ACh content (Fig.   4c). [score:3]
In the present study, we measured the levels of IA-2 and miR-342 in two SCLC cell lines, and then inhibited IA-2 by siRNA transfection and altered miR-342 levels with mimics and inhibitors to determine their effect on SCLC growth and ACh levels. [score:3]
The optimal concentration of ACh was selected, and then added to the NCI-H82 cells treated with scramble siRNA, IA-2 siRNA, miR-342 mimic, or the miR-342 inhibitor. [score:3]
After transfecting the NCI-H82 and NCI-H345 cells with either the IA-2 siRNA, miR-342 mimic, or the miR-342 inhibitor, the cells were incubated for 4 days, and then the cells and supernatants were collected [6, 7]. [score:3]
In brief, after the cells were subjected to the different treatments (transfection with IA-2 siRNA or miR-342 mimic or inhibitor), they were cultured for up to 4 days. [score:3]
To confirm that the effect of IA-2 siRNA and miR-342 on SCLC cell proliferation is mediated through the ACh autocrine growth loop, ACh was added to the culture medium of the NCI-H82 cells that were treated with either the scrambled siRNA, IA-2 siRNA, miR-342 mimic, or the miR-342 inhibitor. [score:3]
Our studies show for the first time that both miR-342 and its target gene IA-2 are involved in the growth process of SCLC cells and act by their effect on autocrine secretion. [score:3]
In contrast, the miR-342 inhibitor produced a slight but significant increase in SCLC cell proliferation at 4 days after transfection (Fig.   4a, b). [score:3]
Taken together, these findings show for the first time, that the neurotransmitter ACh is effective in rescuing the inhibitory effects of siRNA and miR-342 on cell proliferation. [score:3]
Predesigned siRNAs (Hs_PTPRN_3, 4, 5, 6) against human IA-2 (NM_001199763, NM_001199764, NM_002846), scrambled negative control, miR-342 mimic, miR-342 inhibitor, and HiPerFect Transfection Reagent were obtained from Qiagen. [score:3]
Growth curve analysis showed that NCI-H82 and NCI-H345 cells treated with the miR-342 mimic significantly suppressed SCLC cell proliferation by as much as 30 % (Fig.   4a, b). [score:3]
b Similarly, the inhibitory effect of miR-342 on NCI-H82 cell growth is reduced by ACh treatment (1 mM). [score:3]
Fig.  5ACh rescues the inhibitory effect of IA-2 siRNA and miR-342 mimic on SCLC cell growth. [score:3]
Finally, the addition of ACh to cells that had been treated with the miR-342 inhibitor produced an increase in cell proliferation with the greatest magnitude compared to the other treatment conditions (Fig.   5b). [score:2]
SCLC cell growth was evaluated following the knockdown of endogenous IA-2 with RNAi or by overexpressing miR-342 with a mimic. [score:2]
The knockdown of IA-2 by RNAi or miR-342 with a mimic also resulted in a significant decrease in the secretion of ACh, one of the autocrine hormones secreted by SCLC. [score:2]
Similarly, the addition of ACh to cells treated with the miR-342 inhibitor produced an increase in cell proliferation with the greatest magnitude compared to the other treatment conditions. [score:2]
The underlying role of miR-342 in the pathogenesis of lung cancer, however, remains unclear. [score:1]
Both NCI-H82 and NCI-H345 cells transfected with the miR-342 mimic showed a significant reduction in ACh cell content and secretion (Fig.   4c–f). [score:1]
Similar results were obtained when these cell lines were transfected with a miR-342 mimic. [score:1]
Similarly, ACh produced a highly significant increase in the proliferation of cells that had been treated with miR-342 mimic (Fig.   5b). [score:1]
a, b Cell growth rates (based on cell count), were significantly reduced in both NCI-H82 and NCI-H345 cell lines transfected with the miR-342 mimic. [score:1]
Fig.  6 Schematic representation of the effects of IA-2 siRNA and miR-342 mimic on SCLC cell proliferation through ACh autocrine function SCLC is an aggressive malignancy with a distinct natural history and poor prognosis, leading to the death of approximately 16,000 patients per year in United States. [score:1]
ACh secretion levels (e, f), and intracellular ACh content (c, d), were measured in both NCI-H82 and NCI-H345 cells after transfecting with either the miR-342 mimic or the miR-342 inhibitor 4 days post-transfection. [score:1]
Further studies revealed that the growth of SCLC cell lines that had been treated with the miR-342 mimic was restored to nearly normal levels by treatment with ACh. [score:1]
Quantitative RT-PCR for both mRNA and miRNA was performed using the miScript II RT kit, and then the miScript SYBR Green PCR kit for measuring miR-342 expression, or SYBR Green PCR Master Mix for measuring the expression of IA-2 and GAPDH (glyceraldehyde-3-phosphate dehydrogenase) mRNA with a 7500 Real-Time PCR system (Applied Biosystems). [score:1]
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6
[+] score: 91
In addition, miR-342-3p was substantially downregulated in patients with primary myelofibrosis, polycythemia vera, or essential thrombocythemia [43], and specifically upregulated in acute promyelocytic leukemia cell lines during retinoic acid -induced differentiation [44]. [score:7]
The results, normalized for the expression of the housekeeping Z30 small nucleolar RNA, are reported in additional file 2. Specifically, we found appreciable levels of expression for miR-335, miR-342-3p, and miR-628, whereas mir-561 and mir-559 were moderately expressed. [score:7]
The expression levels of the six genes are shown in Fig. 1. Table 1 Selected HG-U133A probes with average fold-change higher than two in HMCLs HG-U133A probe Host gene Host gene intron Intron length (bp) Strand direction miRNA Location Fold-change 222156_x_at CCPG1 intron 5 4,903 - miR-628 15 q21 2.3 217838_s_at EVL intron 3 25,879 + miR-342 14q32 2.7 204235_s_at GULP1 intron 1 90,649 + miR-561 2q32 4.3 204237_at GULP1 4 215913_s_at GULP1 2.5 202016_at MEST intron 2 1,632 + miR-335 7q32 4.8 201839_s_at TACSTD1 intron 5 1,874 + miR-559 2p 9.7 211828_s_at TNIK intron 21 5,584 - miR-569 3q26 3 213107_at TNIK 2.4 213109_at TNIK 2.3 Figure 1 Host gene expression levels. [score:6]
The expression levels of the six genes are shown in Fig. 1. Table 1 Selected HG-U133A probes with average fold-change higher than two in HMCLs HG-U133A probe Host gene Host gene intron Intron length (bp) Strand direction miRNA Location Fold-change 222156_x_at CCPG1 intron 5 4,903 - miR-628 15 q21 2.3 217838_s_at EVL intron 3 25,879 + miR-342 14q32 2.7 204235_s_at GULP1 intron 1 90,649 + miR-561 2q32 4.3 204237_at GULP1 4 215913_s_at GULP1 2.5 202016_at MEST intron 2 1,632 + miR-335 7q32 4.8 201839_s_at TACSTD1 intron 5 1,874 + miR-559 2p 9.7 211828_s_at TNIK intron 21 5,584 - miR-569 3q26 3 213107_at TNIK 2.4 213109_at TNIK 2.3 Figure 1 Host gene expression levels. [score:6]
With regard to miR-342-3p, solely the EVL itself resulted significantly upregulated in the ten samples overexpressing EVL. [score:6]
Specifically, our data showed that miR-335, miR-342-3p, and miR-561 were overexpressed in a fraction of the pathological samples with respect to normal plasma cells, without correlation to any of the known genetic alterations frequently found in MM; this finding may provide further evidence of the genetic complexity of this disease. [score:5]
For three miRNAs, miR-335, miR-342-3p, and miR-561, we demonstrated coordinated expression with their cognate protein-coding genes MEST, EVL, and GULP1; conversely, we did not find correlated expression of miR-628 and miR-559 and their host genes CCPG1 and TACSTD1. [score:5]
One can speculate that miR-342-3p and EVL deregulation may target plasma cell homing into the bone marrow and/or interactions with the bone marrow microenvironment, much the same as for miR-335. [score:4]
In addition, despite the fact that miR-335 deregulation in melanoma and ovarian carcinoma was reported to be concordant with CN gain [39], neither miR-335 nor miR-342-3p and miR-561 expression levels were significantly correlated with their corresponding locus CN in our panel of HMCLs tested by SNPs arrays. [score:4]
Notably, although we tested only a limited number of samples, we found a significant correlation in expression with the corresponding host genes for miR-335, miR-342-3p, and miR-561 (R = 0.95 at p value = 5.03E-09, R = 0.7 at p value = 5E-03, and R = 0.78 at p value = 2E-04, respectively). [score:3]
As described in additional file 3, the bioinformatic target prediction for miR-335, miR-342-3p, and miR-561 suggests that they might play an important role in proliferation, cell cycle control, cellular migration, and angiogenesis. [score:3]
Expression levels of miR-335, miR-342-3p, and miR-561 correlate with those of their corresponding host genes in HMCLs. [score:3]
Interestingly, miR-335 and miR-342-3p were recently reported to be involved in human cancer; depleted expression of miR-335 was found to be associated with metastatic processes in human breast cancer. [score:3]
miR-335, miR-342-3p, and miR-561 are overexpressed in primary MM tumors. [score:3]
With regard to miR-342-3p, it is usually expressed in a variety of human tissues, together with its host gene EVL. [score:3]
Intriguingly, EVL is an actin -associated protein that is involved in a variety of processes related to cytoskeleton remo deling and cell polarity [45]; among miR-342-3p predicted targets, we recognized genes involved in actin cytoskeleton organization and biogenesis (FHL3 and, again, RASA1). [score:3]
This approach led to the identification of three miRNAs (miR-335, miR-342-3p, and miR-561) that were differentially expressed, along with their corresponding host genes, in the dataset of HMCLs. [score:3]
The predicted putative miRNA targets and the transcriptional profiles associated with the primary tumors suggest that MEST/miR-335 and EVL/miR-342-3p may play a role in plasma cell homing and/or interactions with the bone marrow microenvironment. [score:3]
Transcriptional profile associated with miR-335, miR-342-3p, and miR-561 overexpression. [score:3]
A regression analysis of Q-RT-PCR miRNA values and microarray expression levels of matching host genes, conducted with R packages/software, revealed a significant correlation with the corresponding host genes for miR-335, miR-342-3p, and miR-561 (R higher than 0.6 in all cases with a p value < 0.005; see Fig. 2), but not for miR-559 (R = 0.12 at p value = 0.60) or miR-628 (R = 0.32 at p value = 0.15). [score:3]
We evaluated the expression levels of the corresponding intronic miRNAs and identified a significant correlation between the expression levels of MEST, EVL, and GULP1 and those of the corresponding miRNAs miR-335, miR-342-3p, and miR-561, respectively. [score:3]
miR-335, miR-342-3p, and miR-561 deregulations are not associated with genomic alterations. [score:2]
Specifically, we found the following pairs of host genes and intronic miRNAs: CCPG1 (cell cycle progression 1) and miR-628; GULP1 (engulfment adaptor PTB domain containing 1) and miR-561; MEST (mesoderm specific transcript homolog, mouse) and miR-335; EVL (Enah/Vasp-like) and miR-342-3p; TACSTD1 (tumor -associated calcium signal transducer 1) and miR-559; and TNIK (TRAF2 and NCK interacting kinase) and miR-569 (details in Table 1). [score:1]
Notably, miR-335, miR-342-3p, miR-561, and miR-559, but not miR-628, are sense oriented with respect to the corresponding host gene. [score:1]
As specified in Table 1, miR-335, miR-342-3p, miR-561, and miR-559 are all sense oriented, whereas miR-628 is in an antisense orientation with respect to its host gene. [score:1]
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7
[+] score: 82
The plasma expression level of let-7d, miR-150, miR-339, and miR-342 was down-regulated whilst that of let-7b, and miR-523 was up-regulated in the AML group at diagnosis compared to healthy controls. [score:8]
The plasma expression level of let-7d, miR-150, miR-339, and miR-342 was down-regulated whilst that of let-7b, and miR-523 was up-regulated in the AML group compared to healthy controls (Figure 1). [score:8]
Among these miRs, two were upregulated (Let-7b, miR-523) and four were downregulated (let-7d, miR-150, miR-339, and miR-342). [score:7]
Among those eight microRNAs, seven were confimed by qRT-PCR; let-7b and miR-523 were upregulated whilst others were downregulated including the two highly significant microRNAs, miR-150, and miR-342. [score:7]
showed that the plasma expression level of miR-150 and miR-342 was similar to that of healthy controls while it was still upregulated compared to AML patients at diagnosis (Figure 6) thus making these two microRNAs as additional novel biomarkers for AML. [score:5]
Among these microRNAs, miR-150, and miR-342 were very significantly downregulated in the plasma of AML patients as confirmed using ROC curve analysis (AUC of 0.835 and 0.8125) that revealed that miR-150, and miR-342 were promising candidate biomarkers for AML at diagnosis. [score:4]
Moreover, we compared the difference in let-7b, let-7d, miR-150, miR-339, miR-342, and miR-523 expression between AML patients and healthy controls and obtained the same differences in their expression regardless of whether cel-miR-39 or miR-16 was used as the normalizer (Figure 3), which further supports that miR-16 is a stable reference in this study. [score:4]
MiR-150 (A, B) and miR-342 (C, D) expression levels were assessed by qRT-PCR and normalized by cel-miR-39 and hsa-miR-16 respectively in healthy controls and Acute Myeloid Leukemia patients. [score:3]
MiR-150 and miR-342 in CR AML patients showed an expression level similar to that of healthy controls. [score:3]
Figure 6 miR-150 and miR-342 expression levels in Remission AML patients resembles that of healthy controls. [score:3]
Plasma miR-150 and miR-342 expression levels in remission AML patients and healthy controls were assessed by qRT-PCR. [score:3]
Figure 3 Relative plasma miR-150 and miR-342 expression levels normalized by cel-miR-39 and hsa-miR-16. [score:3]
In summary, we have shown that the expression level of miR-150 and miR-342 in plasma is associated with diagnosis of AML in human. [score:3]
Figure 4 miR-150 and miR-342 expression levels do not vary between the first and second sampling. [score:3]
Our results have revealed the presence of two microRNAs (miR-150, miR-342) whose levels were very significantly downregulated in the plasma of AML patients at diagnosis compared to healthy controls. [score:3]
Plasma miR-150 and miR-342 expression levels in the first sampling and second sampling were assessed by qRT-PCR. [score:3]
ROC curve analyses revealed that both plasma miR-150 and miR-342 could serve as valuable biomarkers for differentiating AML from controls with an AUC (the areas under the ROC curve) of 0.835 (95% CI: 0.7119– 0.9581; P<0.0001) and 0.8125 (95% CI: 0.6796–0.9454; P=0.0005), respectively (Figures 5A and 5B). [score:1]
ROC curve analyses revealed an AUC (the areas under the ROC curve) of 0.835 (95% CI: 0.7119– 0.9581; P<0.0001) and 0.8125 (95% CI: 0.6796–0.9454; P=0.0005) for miR-150, and miR-342 respectively. [score:1]
Plasma miR-150 yielded an AUC (the areas under the ROC curve) of 0.835 (95% CI: 0.7119– 0.9581; P<0.0001) with 80% sensitivity and 70% specificity in discriminating AML (A), and plasma miR-342 yielded AUC of 0.8125 (95% CI: 0.6796–0.9454; P=0.0005) with 70% sensitivity and 85% specificity (B) in discriminating AML. [score:1]
On the other hand, an important report [36] related to miR-342 demonstrated the importance of its decreased plasma level in breast cancer, particularly in resistance to certain agents. [score:1]
Thus, it might be possible that cancer cells specifically take in the exosome that contains miR-150 and miR-342 and as a result, miR-150 and miR-342 decrease in the plasma. [score:1]
Diagnostic accuracy of plasma miR-150 and miR-342 in AML. [score:1]
At the cut-off value less than 1.146 for miR-342, the sensitivity and the specificity were 70% and 85%, respectively. [score:1]
Our findings indicated that plasma miR-150 and miR-342 are novel important promising biomarkers in the diagnosis of AML. [score:1]
In that respect, the rebound in CR AML patients of miR-150 and miR-342 at the healthy controls’ levels is of particular significance in the perspective of their use as diagnostic and prognostic factors. [score:1]
Present knowledge does not involve circulating miR-150 and miR-342 as references in other human cancers [48, 49]. [score:1]
The ROC curve analysis was used to analyze the diagnostic accuracy of plasma miR-150 and miR-342. [score:1]
ROC curve analyses revealed that plasma miR-150 and miR-342 could serve as valuable biomarkers for differentiating AML from controls. [score:1]
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8
[+] score: 78
Decreased expression of miR-342 in the therapeutically challenging triple -negative breast tumours, increased miR-342 expression in the luminal B tumours, and downregulated miR-520g in ER and PR -positive tumours indicates that not only is dysregulated miRNA expression a marker for poorer prognosis breast cancer, but that it could also present an attractive target for therapeutic intervention. [score:13]
The response graphs for miR-342, miR-520g and miR-520d* in relation to ER, PR and HER2/ neu status, respectively, are shown in Figure 4. Some miRNAs showed that with increased expression, the probability of receptor positivity increased; conversely, other miRNAs showed that with increased expression, the likelihood of the sample being classed as receptor -positive decreased. [score:5]
In the present study, miR-342 has emerged as a potential candidate for regulation of ER/HER2/ neu expression that warrants further functional investigation to elucidate its mRNA targets and its precise role in breast carcinogenesis. [score:4]
Figure 7Expression of miR-342 and miR-520g in breast tumours. [score:3]
RQ-PCR of mature miR-342 in these samples showed no significant difference in expression between tumour and tumour -associated normal tissue (P = 0.6, paired t test). [score:3]
In vitro studies have demonstrated that introduction of a hsa-miR-342 mimic to colorectal cancer cells induces apoptosis, suggesting a potential tumour suppressor role for this miRNA [42]. [score:3]
Furthermore, the expression patterns and phenotypic associations of the top-ranking miRNAs miR-342 and miR-520g were validated in an independent sample set of 95 tumours (Figure 7). [score:3]
Expression of miR-342 in the larger cohort of breast tumours (n = 95) using RQ-PCR confirmed the microarray findings of an association between miR-342 and ER positivity. [score:3]
miR-342 expression was also higher in the HER2/ neu -positive tumours (n = 59) versus the HER2/ neu -negative tumours (n = 32) (P = 0.001, independent t test). [score:3]
A recent study has shown downregulation of miR-342 in tamoxifen-resistant breast cancer cells compared with tamoxifen-sensitive breast cancer cells, suggesting a potential role as a biomarker of drug sensitivity [65]. [score:3]
The expression of miR-342 was highest in the luminal B subtype of breast cancers and was lowest in the triple -negative/basal subtype (P = 0.001, analysis of variance; Figure 7). [score:3]
Our findings of increased miR-342 expression in both ER -positive and HER2/ neu -positive tumours is of particular interest as the luminal B (ER [+]/HER2/ neu [+]) and triple -negative tumours present particular therapeutic challenges. [score:3]
MiR-342 and miR-520g expression was further analysed in 95 breast tumours. [score:3]
The expression of miR-342 was further analysed in a cohort of 95 breast tumours, 17 of which had matched tumour -associated normal tissue. [score:3]
The miRNA signatures generated for ER status (miR-342, miR-299, miR-217, miR-190, miR-135b, miR-218), for PR status (miR-520g, miR-377, miR-527-518a, miR-520f-520c) and for HER2/ neu status (miR-520d, miR-181c, miR-302c, miR-376b, miR-30e) include miRNAs that have previously been identified as dysregulated in breast cancer and other cancers [7, 9, 37- 43] and involved in the regulation of cell functions such as growth, apoptosis, migration and invasion [38, 42, 43]. [score:3]
Increasing evidence suggests that miR-342 plays an important role in the carcinogenic process, particularly in the hormonally regulated breast cancer. [score:2]
Within the tumour samples, the expression of miR-342 was significantly higher in ER -positive tumours (n = 62) compared with ER -negative tumours (n = 32) (P = 0.04, independent t test), confirming the association with ER positivity identified in the ANN response curve analysis. [score:2]
MiR-342 expression was highest in ER and HER2/ neu -positive luminal B tumours and lowest in triple -negative tumours. [score:2]
Notably, two chromosomal locations account for a number of the dysregulated miRNAs in these predictive sets: Ch19q13 (miR-520g, miR-520d, miR-527-528a, miR-520f-520c, miR-181c) and Ch14q32 (miR-342, miR-299, miR-377, miR-376b). [score:2]
miR-342 is dysregulated in multiple myeloma [64] and has been shown to be epigenetically silenced by methylation in colorectal carcinoma [42]. [score:2]
RQ-PCR detection analysis shows that expression levels of miR-342 are increased in: (a) oestrogen receptor (ER) -positive tumours compared with ER -negative tumours (P = 0.04), (b) v-erb-b2 erythroblastic leukaemia viral oncogene homolog 2 receptor (HER2/ neu) -positive compared with HER2/ neu -negative tumours (P = 0.001), and (c) luminal-B subtype of breast tumours (P = 0.001). [score:1]
Furthermore, we report the first findings of an association between miR-342 and HER2/ neu positivity. [score:1]
The first miRNA identified by the ANN mo del in relation to ER status was miR-342. [score:1]
To our knowledge this is the largest number of primary breast tumours in which miR-342 has been quantitated using RQ-PCR. [score:1]
Response curves for (a) miR-342, (b) miR-520g and (c) miR-520d*. [score:1]
Figure 4Response curves for miR-342, miR-520g and miR-520d. [score:1]
Previous miRNA profiling studies in breast cancer have identified associations between miR-342 and ER, intrinsic breast cancer subtype and tumour grade [7, 9]. [score:1]
Stepwise ANN analysis identified predictive miRNA signatures corresponding with oestrogen (miR-342, miR-299, miR-217, miR-190, miR-135b, miR-218), progesterone (miR-520g, miR-377, miR-527-518a, miR-520f-520c) and HER2/ neu (miR-520d, miR-181c, miR-302c, miR-376b, miR-30e) receptor status. [score:1]
There was no association of miR-342 with other clinicopathological parameters, including PR status, grade, stage or nodal status. [score:1]
The ER signature consisted of six miRNA transcripts (miR-342, miR-299, miR-217, miR-190, miR-135b, miR-218), and discriminated cases correctly with a median accuracy of 100% when classifying between ER -positive and ER -negative phenotypes. [score:1]
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9
[+] score: 76
However, given that hsa-miR-342-3p was found in two experimental animal mo dels and in human Creutzfeldt-Jakob disease, we assume that this miRNA may play a general role in the regulation of multiple target genes in late-stage prion disease. [score:8]
Although regulation of hsa-miR-342-3p was not observed in miRNA studies using brain samples from Alzheimer's [26], or Huntington's disease [9] patients, we cannot rule out that this miRNA is not exclusively upregulated in prion -induced disorders. [score:7]
Analysis of the target predictions for hsa-miR-342-3p and hsa-miR-494 as revealed by the public target prediction program TargetScan (release 5.1, April 2009) for involvement in neurodegeneration and neurodegenerative disorders. [score:7]
In this case hsa-miR-342-3p would also be upregulated in human prion disease. [score:6]
Beside others, putative target genes involved in neurodegenerative diseases were found for both, hsa-miR-342-3p and hsa-miR-494. [score:5]
However, our analysis revealed that both miRNAs, hsa-miR-342-3p and hsa-miR-494, were significantly upregulated in BSE-infected macaques (Table 1). [score:4]
However, the comparable regulation of hsa-miR-342-3p may apply to prion disease in general. [score:4]
Among others, such as hsa-miR-191, hsa-miR-200b, hsa-miR-320 and several members of let-7 family we found that hsa-miR-342-3p was regulated at a late stage of disease in both, Scrapie-infected mice and BSE-infected macaques. [score:4]
Our pilot study revealed that hsa-miR-342-3p was upregulated approximately 2-fold in sCJD type 1 and 1.5-fold in sCJD type 2, respectively (Figure 2B) at a comparable level as in BSE-infected macaques. [score:4]
To strengthen our hypothesis we assessed the regulation of miR-342-3p in brains of sporadic Creutzfeldt-Jakob disease (sCJD) patients. [score:4]
Analysis of predicted targets for hsa-miR-342-3p and hsa-miR-494. [score:3]
The relative expression of selected miRNA candidates hsa-miR-26a, hsa-miR-124a, hsa-miR-143, hsa-miR-145, hsa-miR-342-3p, and hsa-miR-494 were validated by quantitative reverse transcription PCR (qRT-PCR) analysis using a higher number of animals. [score:3]
C [T]-values derived from 4 independent qRT-PCR experiments comparing the expression of miRNAs hsa-miR-26a, hsa-miR-124a, hsa-miR-143, hsa-miR-145, hsa-miR-342-3p, and hsa-miR-494 in BSE-infected vs. [score:3]
Click here for file Analysis of predicted targets for hsa-miR-342-3p and hsa-miR-494. [score:3]
The miR-342-3p expression in the brains of a sCJD type 1 and a sCJD type 2 patient compared to a non-infected individual was analysed by qRT-PCR. [score:2]
Figure 2 Regulation of miRNA hsa-miR-342-3p in different prion disorders. [score:2]
B. Regulation of miR-342-3p in samples derived from brains of patients with type 1 sCJD, type 2 sCJD and a healthy control, respectively. [score:2]
In addition, we only assessed the expression of hsa-miR-342-3p in two sCJD patients which was compared to one healthy control. [score:2]
MiRNA was enriched as described for simian brains and applied to stem-loop qRT-PCR for hsa-miR-342-3p. [score:1]
Since the mature forms of hsa-miR-342-3p and miR-494 reside on the 3'-arm of the pre-miRNA the stem-loop qRT-PCR cannot distinguish between DICER processed or unprocessed forms. [score:1]
5 ng miRNA were applied to qRT-PCR specific for hsa-miR-342-3p (stem-loop qRT-PCR, Applied Biosystems). [score:1]
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[+] score: 65
The up-regulated and down-regulated miRNAs (miR-20b, miR-92a-3p, miR-92b, miR-376c-3p, miR-150, miR-342-3p, and miR-663) may be involved in the regulation of transcription, DNA -dependent positive regulation of transcription from RNA polymerase II promoter, protein amino acid phosphorylation, and negative regulation of transcription from RNA polymerase II promoter. [score:10]
Moreover, lower expression of miR-150 and miR-342-3p up-regulated Bcl-2–associated X protein and CASP8 and FADD-like apoptosis regulator (CFLAR), which have apoptotic activities [49, 53]. [score:7]
b Relationship among target genes predicted by miR-150, miR-342-3p, and miR-663 Fig. 5GO and pathway analysis result of the target genes predicted by differentially expressed miRNAs which are involved in HBV -induced HCC. [score:7]
In addition, all down-regulated miRNAs (miR-150, miR-342-3p, and miR-663) target baculoviral IAP repeat containing 5 (BIRC5), CCND1, and protein tyrosine kinase 2 (PTK2). [score:6]
All down-regulated miRNAs (miR-150, miR-342-3p, and miR-663) target B-cell lymphoma/leukemia 2 (BCL2), BIRC5 and PTK2. [score:6]
Similarly, the processes targeted by at least two of several miRNAs (miR-150, miR-342-3p, and miR-663) were cellular response to starvation, positive regulation of transcription from RNA polymerase II promoter, regulation of transcription, DNA -dependent protein amino acid phosphorylation, and negative regulation of transcription from RNA polymerase II promoter (Fig.   5b). [score:6]
The predicted target genes of miR-150, miR-342-3p, and miR-663 were related to MAPK signaling pathway, cytokine-cytokine receptor interaction, focal adhesion, insulin signaling pathway, and regulation of actin cytoskeleton (Fig.   5d). [score:4]
Our data indicates that the unique 7 miRNAs (miR-150, miR-342-3p, miR-663, miR-20b, miR-92a-3p, miR-376c-3p and miR-92b) expression signature could be involved in the development of HBV- related HCC, suggesting interesting potential novel therapeutic options. [score:4]
By miRNA expression profile, we found that miR-150, miR-342-3p, miR-663, miR-20b, miR-92a-3p, miR-376c-3p, and miR-92b are specifically altered in HBV-related HCC. [score:3]
b Main biological processes influenced by genes targeted by two or more miRNAs from miR-150, miR-342-3p, and miR-663. [score:3]
IPA-obtained network showing the relationships among 6 co-regulated miRNAs (miR-150, miR-342-3p, miR-92a-3p, miR-92b, and miR-376c-3p) To evaluate the effect of HBV infection on the change in expression of miRNAs, 12 pairs of samples from HCC and non-tumor tissues (including 6 HBV -positive HCC and 6 HBV -negative HCC and their non-tumor tissues) were collected. [score:2]
IPA-obtained network showing the relationships among 6 co-regulated miRNAs (miR-150, miR-342-3p, miR-92a-3p, miR-92b, and miR-376c-3p) HBV infection is a major health problem that leads to a significant rise in mortality and is reported to be closely related to HCC [20]. [score:2]
In our study, a network that includes 6 of 7 selected miRNAs (miR-150, miR-342-3p, miR-20b, miR-92, miR-368, and miR-92b) was shown based on accepted databases of molecular interactions reported in the literature using IPA (Fig.   6). [score:1]
The identity of the 12 miRNAs is as follows: miR-21, miR-20b, miR-92a-3p, miR-92b, miR-376c-3p, miR-150, miR-451, miR-101, miR-424, miR-342-3p, miR-122a, and miR-663. [score:1]
Ultimately, miR-20b, miR-92a-3p, miR-92b, miR-376c-3p, miR-150, miR-342-3p, and miR-663 were selected. [score:1]
Eight miRNAs (miR-223, miR-98, miR-15b, miR-199a-5p, miR-19b, miR-22, miR-451, and miR-101) were involved in HBV-unrelated HCC, 5 miRNAs (miR-98, miR-375, miR-335, miR-199a-5p, and miR-22) were involved in HBV infection, and 7 miRNAs (miR-150, miR-342-3p, miR-663, miR-20b, miR-92a-3p, miR-376c-3p and miR-92b) were specifically altered in HBV-related HCC. [score:1]
In our IPA results, the 6 selected miRNAs (miR-150, miR-342-3p, miR-20b, miR-92a-3p, miR-92b, and miR-376c-3p) are shown to comprise a network which linked themselves among AGO2, DICER1, BCL2L11, CCND1, CCND2, CCNE1, CDK7, E2F1, E2F3, TP53, and four other genes (Fig.   6). [score:1]
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[+] score: 57
Indeed, among CC founder strains, we found a strong correlation between miR-342-3p and miR-342-5p expression, with NOD/ShiLtJ and PWK/PhJ strains having low expression for both arms of miR-342 (Additional file 1: Figure S4). [score:5]
We suggest that rs264778660 affects the maturation and expression of miR-342-3p, providing a plausible explanation for why preCC mice with haplotypes at this locus matching that of NOD/ShiLtJ and PWK/PhJ have lower expression levels. [score:5]
Taken together, these results indicate that cis-regulatory elements at the respective eQTL are the primary determinants of miR-489 and miR-342-3p expression in the lung. [score:4]
We estimated the broad sense heritability (H [2]) for miRNA expression (Additional file 5: Table S2); H [2] values ranged from 0.28 for miR-200a to 0.94 for miR-342-3p. [score:3]
The red line denotes the branch that contains the putative causal variant The allele effects for miR-342-3p indicated that the NOD/ShiLtJ and PWK/PhJ alleles were similar in terms of their effect on miRNA expression (Fig.   4b). [score:3]
We noted that in del (rs261236356) is predicted to cause a change in the seed sequence of miR-342-5p (Fig.   5), potentially altering the relationship between this miRNA and target genes. [score:3]
Expression of miR-342-3p and miR-342-5p in CC founder lines. [score:3]
These results suggest that at least rs264778660 is likely to cause a change in pre-miR-342 structure, which in turn may alter processing by Dicer and Drosha, and consequently affect expression of both miR-342-3p and miR-342-5p. [score:3]
We did not measure the expression of miR-342-5p in the preCC because its expression levels were very low. [score:3]
a. Expression of miR-342-3p in CC founders (a) and preCC mice (b) as a function of founder haplotype at the eQTL on chromosome 12. [score:3]
The red line denotes the branch that contains the putative causal variantThe allele effects for miR-342-3p indicated that the NOD/ShiLtJ and PWK/PhJ alleles were similar in terms of their effect on miRNA expression (Fig.   4b). [score:3]
Two SNPs (rs264778660 and rs242689107) and one in del (rs261236356) were in the miR-342 precursor (pre-miR-342) and thus were considered strong candidate causal variants for the eQTL because the stem-loop structure of the precursor is critical for miRNA maturation and expression. [score:2]
The predicted structure of pre-miR-342 with the addition of the in del (rs261236356) is shown at right Seven other miRNAs had local eQTL: miR-146b, miR-181d, miR-187, miR-203, miR-221, miR-322, and miR-503. [score:1]
The RNAfold algorithm [35] predicted an allele -dependent effect for both SNPs (but not the in del) on the terminal loop of the pre-miR-342 stem-loop structure (Fig.   5). [score:1]
Black diamonds represent means by strain or haplotype Fig. 4 The miR-342-3p eQTL. [score:1]
One of the largest-effect local miRNA eQTL was for miR-342-3p, for which we identified putative causal variants by bioinformatic analysis of the effects of single nucleotide polymorphisms on RNA structure. [score:1]
SNP positions refer to miR-342-3p precursor as shown in Fig.   5. Figure S4. [score:1]
Predicted effects of SNPs in miR-342-3p on miR-342 structure as determined by SNPfold. [score:1]
c. Phylogeny of CC founder strains based on SNP data for the region on Chr 12 containing the miR-342-3p eQTL. [score:1]
The predicted structure of pre-miR-342 with the addition of the in del (rs261236356) is shown at rightSeven other miRNAs had local eQTL: miR-146b, miR-181d, miR-187, miR-203, miR-221, miR-322, and miR-503. [score:1]
Two eQTL, for miR-489 and miR-342-3p, stood out in terms of effect size. [score:1]
Fig. 5Predicted effects of SNPs in miR-342 on pre-miR-342 structure. [score:1]
We identified 938 SNPs in the region that met these criteria, the majority of which were located in or near 11 genes (defined as +/− 5 kb from the gene), including 20 SNPs in or near the miR-342 locus. [score:1]
Subsequent analysis using SNPfold [36] provided further in silico evidence that rs264778660 significantly alters the conformation of pre-miR-342 (p = 0.01, Additional file 1: Figure S3). [score:1]
We found that a SNP (rs264778660) located in the miRNA precursor is likely to alter the terminal loop of the pre-miR-342 structure, which in turn may alter processing and maturation of miR-342-3p. [score:1]
Top: sequence spanning 109,896,830-109,896,928 bp on Chr 12 with miR-342-5p and miR-342-3p sequences shown in blue and green, respectively. [score:1]
Bottom: the sequence of miR-342 from C57BL/6J reference strain was used to generate a structure of pre-miR-342, shown on the left. [score:1]
In the case of miR-342-3p, we were able to identify highly plausible candidate causal variants using a combination of sequence data and structural mo deling. [score:1]
First, we used RNAfold [35] to compare the predicted structures of pre-miR-342 based on the reference allele (C57BL/6J) to a musculus-derived allele (shared by the NOD/ShiLtJ and PWK/PhJ strains) containing two SNPs (rs264778660 and rs242689107) and one in del (rs261236356) that fall within the precursor. [score:1]
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[+] score: 52
It was shown to be upregulated in AD mouse brain and predicted to hamper the function of axon initial segment by decreasing the expression of ankyrin G. Predicted to target BACE1 and IGF2, miR-342-5p may play a significant role in AD. [score:8]
Among these differentially expressed miRNAs, miR-342-3p was consistently upregulated in 1-month-old, 6-month-old, and 9-month-old APP/PS1 mice, which suggests that miR-342-3p may play a role in the process of AD. [score:6]
In these differentially expressed miRNAs, miR-342-3p inhibited cell proliferation, migration, and invasion in osteosarcoma, gliomas, and other cancers [37– 39]. [score:5]
MiR-342-5p, miR-3058-3p, let-7f-5p, miR-1961, miR-301b-3p, miR-98-5p, miR-1251-5p, miR-215-5p, miR-881-5p, miR-135a-2-3p, and miR-33-3p may regulate the expression of insulin-like growth factor 1 (IGF1) or insulin-like growth factor 2 (IGF2), two molecules that could rescue behavior and memory deficits via lowering A β levels [28, 29]. [score:4]
In addition, some differences were found between those results; for example, the level of miR-342-3p was downregulated in AD patient plasma samples, while in our study it was significantly elevated in APP/PS1 mouse brain of 1-month-old, 6-month-old, and 9-month-old mice [46]. [score:4]
miR-376c-3p and miR-342-3p were predicted to affect tau phosphorylation by directly targeting the 3′-UTR of PP2A. [score:4]
miR-342-5p was upregulated in brain tissue of 1-month-old and 6-month-old mice, indicating that it is effective at early onset and therefore may act as a specific early biomarker of AD. [score:4]
Among these miRNAs, miR-342-3p was upregulated from 1-month-old to 9-month-old AD mice, suggesting that it may play a critical role in the entire AD process. [score:4]
Several miRNAs derived from our microarray analysis targeted PTEN, such as miR-376c-3p, miR-342-3p, let-7f-5p, miR-10a-5p, miR-301b-3p, miR-98-5p, miR-1251-5p, and miR-34a-5p. [score:3]
Considering a probe signal of over 100 as abundance, eleven of the 28 miRNAs (miR-342-3p, miR-342-5p, miR-376c-3p, miR-301b-3p, let-7f-5p, miR-539-3p, miR-491-3p, miR-10a-5p, miR-98-5p, miR-652-5p, and miR-34a-5p) were shown to have targets that are tightly related to AD and could easily be detected. [score:3]
miR-342-5p was reported to manage neuron stem proliferation and differentiation by targeting Notch signaling [42]. [score:3]
Moreover, miR-342-5p was elevated in both 1-month-old and 3-month-old APP/PS1 mouse groups, suggesting that miR-342-5p may play a role in early stages of AD. [score:1]
For further analysis, we chose 11 evidently different miRNAs that were conserved between both human and mouse: miR-342-3p, miR-342-5p, miR-376c-3p, miR-301b-3p, let-7f-5p, miR-539-3p, miR-491-3p, miR-10a-5p, miR-98-5p, miR-652-5p, and miR-34a-5p. [score:1]
To our knowledge, this is the first study to identify the potential effects of miR-342-3p, miR-491-3p, miR-539-3p, miR-376c-3p, miR-10a-5p, and miR-652-5p in the progression of AD. [score:1]
Although it is challenging to compare our results to the results of other studies in which different tissues and species were used, several miRNAs, including let-7f-5p, miR-342-5p, and miR-98-5p, showed a similar trend in human blood and CSF [48, 49]. [score:1]
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[+] score: 48
This study describes how p19 affects the RNA world and shows that: i) miR-342, miR-206, miR-330, miR-138 and miR-99b are upregulated by p19 but not by p19W164A mutant; ii) anti-miR-206 can restore the G2 phase in the presence of p19; iii) p19 and p21Q61L regulate their own alternative splicing; iv) miR-206 and miR-138 are differentially regulated by p19 and p21 H-Ras and v) P19G12S Costello mutants show a clear upregulation of miR-374, miR-126, miR-342, miR-330, miR-335 and let-7. These results allow us to conclude that the H-Ras G12S mutation plays an important role in miRNA expression and open up a new line of study to understand the consequences of this mutation on Costello syndrome. [score:13]
We analyzed the obtained miRNAs by the TARGETSCAN tool and observed that miR-330 may target SC-35 and many other SR proteins as well as an UsnRNP core protein, mir-342 may target SF4, and miR-206 may target p68 RNA helicase and many other SR proteins. [score:9]
These miRNAs included miR-342 and miR-330, which are already known to be upregulated by p19 overexpression (Fig.   1), miR-126 and miR-335, which significantly reduce the ability of CN34-LM1 and CN34-BoM1 cells to metastasize to the lung [23], miR-374, which is known to be associated with aggressive small cell lung cancer [26], and let-7, which targets Ras genes [27]. [score:8]
Two of the miRNAs upregulated by p19 (Additional file 1) have previously been reported to be of significant interest in cancer studies: miR-342 is one of the miRNA markers for acute promyelocytic leukemia [30, 31] and miR-206 suppresses ERα in breast cancer cell lines and also plays a role in muscular dystrophy [32– 34]. [score:6]
miRNA upregulation by p19 H-Ras was re-validated by RT-PCR with a specific Taqman assay for mature miR-206, miR-342, miR-138 and miR-330 and was found to increase 2-, 1.6-, 16- and 2.5-fold, respectively, upon overexpression of p19 in three independent experiments and quadruplicate analysis. [score:5]
Thus, p21 was found to upregulate miR-374, miR-126, miR-342, miR-335 and let-7 but not miR-330, and p21G12S was found to have the same effect as p21 on miR-374, miR-342 and miR-126. [score:4]
Candidate miRNAs were found to be miR-342, miR-206, miR-330, miR-138, and mirR-99b (Fig.   1a and 1), which vary with p19 but not with the specific p19mut overexpression. [score:3]
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[+] score: 47
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-16-1, hsa-mir-17, hsa-mir-21, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-27a, hsa-mir-29a, hsa-mir-30a, hsa-mir-98, hsa-mir-101-1, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-106a, hsa-mir-107, hsa-mir-16-2, hsa-mir-198, hsa-mir-148a, hsa-mir-30d, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-181c, hsa-mir-182, hsa-mir-183, hsa-mir-205, hsa-mir-210, hsa-mir-181a-1, hsa-mir-222, hsa-mir-224, hsa-mir-200b, hsa-let-7g, hsa-let-7i, hsa-mir-23b, hsa-mir-27b, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-125b-1, hsa-mir-128-1, hsa-mir-132, hsa-mir-137, hsa-mir-140, hsa-mir-141, hsa-mir-142, hsa-mir-143, hsa-mir-144, hsa-mir-153-1, hsa-mir-153-2, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-134, hsa-mir-136, hsa-mir-146a, hsa-mir-150, hsa-mir-184, hsa-mir-185, hsa-mir-186, hsa-mir-206, hsa-mir-320a, hsa-mir-200c, hsa-mir-128-2, hsa-mir-200a, hsa-mir-101-2, hsa-mir-34b, hsa-mir-34c, hsa-mir-299, hsa-mir-26a-2, hsa-mir-373, hsa-mir-376a-1, hsa-mir-133b, hsa-mir-424, hsa-mir-429, hsa-mir-433, hsa-mir-451a, hsa-mir-146b, hsa-mir-494, hsa-mir-193b, hsa-mir-455, hsa-mir-376a-2, hsa-mir-33b, hsa-mir-644a, hsa-mir-548d-1, hsa-mir-548d-2, hsa-mir-320b-1, hsa-mir-320c-1, hsa-mir-320b-2, hsa-mir-301b, hsa-mir-320d-1, hsa-mir-320c-2, hsa-mir-320d-2, hsa-mir-320e, hsa-mir-3613, hsa-mir-4668, hsa-mir-4674, hsa-mir-6722
Bellingham et al. (2012) demonstrated that let-7b, let-7i, miRNA-128a, miRNA-21, miRNA-222, miRNA-29b, miRNA-342-3p, and miRNA-424 levels were upregulated, while miRNA-146a levels were downregulated in prion-infected individual. [score:7]
Similarly, miR-342-3p and miR-21-5p are upregulated in the brains of sheep naturally infected with prion disease (Sanz Rubio et al., 2017). [score:6]
Upregulation of miRNA hsa-miR-342-3p in experimental and idiopathic prion disease. [score:6]
Although, the TargetScan algorithm shows some important genes targeted by miRNA-342-3p, such as ataxin 7, tau tubulin kinase 2 and huntingtin interacting protein 1 (HIP1). [score:5]
Similarly, miRNA-342-3p was also upregulated in scrapie-infected mice brains (Saba et al., 2008; Montag et al., 2009). [score:4]
In addition, the miRNA miRNA-342-3p was also upregulated in the brains of human type 1 and type 2 sporadic CJD patients. [score:4]
Further confirmation of the significance of miRNA-342-3p in prion diseases is required due to the small number of experimental animals and human brains available for the above-mentioned study (two sCJD and one healthy control) (Saba et al., 2008). [score:3]
Through miRNA-microarray and qRT-PCR analysis, two miRNAs miRNA-342-3p and miRNA-494 were significantly upregulated in the brains of BSE-infected macaques compared to non-infected animals. [score:3]
No validation of this hypothesis exists, due to the lack of knowledge about the target mRNAs for miRNA-342-3p. [score:3]
Increased circulating microRNAs miR-342-3p and miR-21-5p in natural sheep prion disease. [score:3]
These studies reveal that miRNA-342-3p might be a potential biomarker in the terminal stage of prion diseases. [score:3]
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[+] score: 44
Notably, exosomal miR-342–3p and miR-1246 induced a pro-metastatic phenotype, including increased cell motility and invasion, and miR-1246 directly targets DENND2D expression by binding to its 3′UTR. [score:6]
A heatmap of the gene expression profiles of miR-342–3p-, miR-1246-, and miR-NC -transfected HOC313-P cells and the highly metastatic HOC313-LM cell line revealed that transfection with miR-342–3p is insufficient to induce a HOC313-LM-like gene expression profile, in contrast to that of miR-1246 (Fig. 4a). [score:5]
Two miRNAs, miR-342-3p and miR-1246, were upregulated in both whole cells and exosomes. [score:4]
Overexpression of miR-342–3p and miR-1246 enhanced the migration and invasion ability in HOC313-P, TSU and HeLa cells (Fig. 3f, g, Supplementary Fig. S4, S5). [score:3]
Although migration and invasion abilities of HOC313-P, TSU and HeLa cells were increased upon overexpression of miR-342–3p and/or miR-1246, we did not observe any significant effect on cell growth rates. [score:3]
To this end, we performed gene expression array analysis on HOC313-LM cells and on miR-NC-, miR-342–3p- or miR-1246 -transfected HOC313-P cells. [score:3]
We also examined the migration and invasion ability of HOC313-P, TSU and HeLa cells by overexpressing miR-342–3p and/or miR-1246. [score:3]
MicroRNA expression levels of miR-342-3p (left) and miR-1246 (right) relative to the negative controls are shown. [score:3]
Consistent with the miRNA transfer observed in LM-exosome -treated cells, the expression levels of miR-342 and miR- 1246 increased when HOC313-LM cells were in the upper chamber relative to when HOC313-P cells were in the upper chamber (Fig. 3c). [score:3]
These data suggest that a specific miRNA population could be selectively sorted into the exosomes, of which miR-342–3p and miR-1246 could act as oncomiRs in oral squamous cell carcinoma. [score:1]
Exosomal miRNAs miR-342-3p and miR-1246 increase cell motility but not cell growth in HOC313-P, TSU and HeLa cellsFollowing the observation that LM-exosomes function in an oncogenic manner in HOC313-P cells, we hypothesized that the miRNA cargo of LM-exosomes was responsible for such biological functions. [score:1]
Interestingly, we show evidence that the abundance of oncogenic miR-342–3p and miR-1246 in cancer exosomes is significantly associated with malignancy. [score:1]
Gain-of-function was simulated by using miRNA mimics (miR-342- 3p [MC12328], miR-1246 [MC13182] and negative control [4464058]) purchased from Thermo Fisher Scientific. [score:1]
Taken together, these data suggest that miR-342–3p and miR-1246 delivered via LM-exosomes act as oncomiRs by affecting the cell motility of the recipient cells. [score:1]
LM-exosomes contain oncomiRs miR-342–3p and miR-1246 that are transferred to HOC313-P cells for intercellular communication. [score:1]
To test the functions of miR-342-3p and miR-1246, we transiently transfected miR-342–3p and/or miR-1246 into HOC313-P, TSU and HeLa cells. [score:1]
In addition, to examine whether miR-342–3p and miR-1246 transfer requires direct cell contact, we set up a Transwell assay in which HOC313-P cells or HOC313-LM cells were separated from HOC313-P cells by a porous 1-μm upper membrane in a ratio of 4:1. Under this condition, only acellular material, such as exosomes or other soluble factors, can migrate across these membranes 13. [score:1]
Exosomal miRNAs miR-342-3p and miR-1246 increase cell motility but not cell growth in HOC313-P, TSU and HeLa cells. [score:1]
LM-exosomes contain oncomiRs miR-342–3p and miR-1246 that are transferred to HOC313-P cells for intercellular communicationRNA and proteins contained in exosomes contribute to exosome function 21. [score:1]
Therefore, we focused on the functions of miR-342–3p and miR-1246. [score:1]
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[+] score: 43
To address the significance of regulation of telomerase activity by endogenous miRNAs we electroporated inhibitors of miR-138, miR-342, miR-491, and miR-541 into Jurkat cells in which these miRNAs are expressed [42]. [score:6]
miR-342, is downregulated in tamoxifen-resistant breast tumors and in lung carcinomas, inhibits proliferation, invasiveness of colorectal cancer cells, induces apoptosis in cutaneous lymphoma and differentiation of leukemic cells [69]– [73]. [score:6]
These results suggest that endogenous miR-138, miR-342, miR-491, and miR-541 inhibit telomerase activity and their downregulation during tumorigenesis can results in activation of telomerase. [score:6]
The luciferase activity of the WT reporter construct was significantly inhibited in cells transfected with precursors of let-7g*, miR-133a, miR-138, miR-342, miR-491, and miR-541 relative to cells transfected with the negative control. [score:3]
This gene was shown previously to be regulated by miR-138 [55] and our results demonstrated that it is also under regulation of miR-188, miR-342, miR-491, and miR-541. [score:3]
Our report confirms this finding and demonstrates that at least five additional miRNAs (let-7g*, miR-133a, miR-342-5p, miR-491-5p, and miR-541-3p) directly regulate hTERT. [score:3]
Interestingly, the combination of miR-491, miR-541, and miR-342 (MIX1) inhibited telomerase activity more efficiently than any of these miRNAs alone. [score:3]
miR-133a, miR-138, miR-188, miR-342, miR-491, and miR-541 were co -transfected into HeLa cells with a reporter plasmid containing the appropriate 3′UTR and their ability to inhibit reporter activity was analyzed as described for the hTERT 3′UTR. [score:3]
The experiments above demonstrated that the transfection of the miRNAs (miR-138, miR-188, miR-342, miR-491, miR-541) inhibit TCF7 and MSI1 3′UTR reporters, therefore, we analyzed their ability to alter the endogenous protein levels of these genes in DLD-1 cells (Figure 5). [score:3]
1, interferon regulatory factor proteins and miR-342 stimulates ATRA -mediated granulocytic differentiation of acute promyelocytic leukemia cells. [score:2]
The inhibitory effect observed for miR-133a, miR-342, miR-491 and miR-541, was completely or almost completely eliminated when the luciferase assays employed the hTERT 3′UTR constructs with mutated binding sites. [score:2]
The mixtures of miRNAs as well as scrambled control (SC) were always at a concentration of 60 nM; MIX1 (miR-491, miR-541, and miR-342), MIX2 (let-7g*, miR-133a, and, miR-138), MIX3 (MIX1+MIX2). [score:1]
The first combination contained three miRNAs (miR-491, miR-541, and miR-342) that have predicted binding sites in both the 3′UTR of hTERT and in the 3′UTRs of the TCF7, MSI1 and PAX5 genes (Figure 1) (MIX1). [score:1]
Overall, miR-342, miR-491, and miR-541 demonstrated the greatest effect on all three reporters which is consistent since the 3′UTR of these genes have multiple predicted binding sites for the miRNAs examined. [score:1]
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[+] score: 34
In our study, CASP3 was significantly upregulated by qRT-PCR analysis (Figure 6) and targeted by the downregulated miRNAs: miR-342-3p, miR-29b, miR-29c, miR-29a, let-7g and miR-30b, which can be expected to develop miRNA -based therapeutics for influenza disease. [score:11]
No validated miRNA targeting Mx1 has been reported; thus, our miRNA target prediction result indicated that Mx1 can be negatively regulated by miR-342-3p and miR-210, which were both down expressed in H1N1 critically ill patients. [score:8]
Schmidt et al. [78] found that miR-146b-5p, miR-150, miR-342-3p and let-7g were downregulated in peripheral blood leukocytes during acute lipopolysaccharide (LPS) induced inflammation, which was similar to our result. [score:4]
We found that EGFR was regulated by miR-342, miR-155, miR-30b, miR-210, miR-192, let-7g, and miR-146b-5p, which were all down expressed in H1N1 critically ill patients. [score:4]
validation of differentially expressed miRNAs and ROC analysisThe microarray data were validated by performing, qRT-PCR for nine miRNAs, including hsa-miR-146b-5p, hsa-miR-148a, hsa-miR-150, hsa-miR-31, hsa-miR-155, hsa-miR-29a, hsa-miR-29b, hsa-miR-342-5p, and hsa-miR-886-3p. [score:3]
The expression of hsa-miR-150, hsa-miR-31, hsa-miR-155, hsa-miR-29a, hsa-miR-29b, hsa-miR-342-5p, and hsa-miR-146b-5p were present in lower abundance, whereas hsa-miR-148a and hsa-miR-886-3p were present in higher abundance in PBMCs from critically ill patients infected with H1N1 influenza virus than that from healthy controls. [score:3]
The microarray data were validated by performing, qRT-PCR for nine miRNAs, including hsa-miR-146b-5p, hsa-miR-148a, hsa-miR-150, hsa-miR-31, hsa-miR-155, hsa-miR-29a, hsa-miR-29b, hsa-miR-342-5p, and hsa-miR-886-3p. [score:1]
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[+] score: 29
Finally, linking differentially expressed miRNAs to their potential differentially expressed target using the algorithm published by Kertesz et al [25] identified a total of 11 potential miRNA-mRNA pairs: COL21A1 (collagen, type XXI, alpha 1; targeted by hsa-miR-155), CYP46A1 (cytochrome P450, family 46, subfamily A, polypeptide 1; targeted by hsa-miR-342-3p), KCNJ1 (potassium inwardly-rectifying channel, subfamily J, member 1; targeted by hsa-miR-155), MADCAM1 (mucosal vascular addressin cell adhesion molecule 1; targeted by hsa-let-7i), MRPS26 (mitochondrial ribosomal protein S26; targeted by hsa-miR-15a), OR2T29 (olfactory receptor, family 2, subfamily T, member 29; targeted by hsa-miR-143), RPS9 (ribosomal protein S9; targeted by hsa-miR-132), SLC10A1 (solute carrier family 10 (sodium/bile acid cotransporter family), member 1; targeted by hsa-miR-31), SLC16A8 (solute carrier family 16, member 8 (monocarboxylic acid transporter 3); targeted by hsa-miR-31), SNTG1 (syntrophin, gamma 1; targeted by hsa-miR-21) and TRPC5 (transient receptor potential cation channel, subfamily C, member 5; targeted by hsa-miR-335). [score:29]
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A) K562 miRNA Host Transcript miRNA:Host transcript Status miR-342 EVL Downregulated miR-548e SHOC2 Downregulated miR-486 ANK1 Upregulated B) HL60 miRNA Host Transcript miRNA:Host transcript Status miR-22 C17orf91 Downregulated miR-151 PTK2 Downregulated miR-199b DNM1 Upregulated miR-25 MCM7 Upregulated miR-618 LIN7A Upregulated The analysis of microarray data revealed induction in the expression of some of the miRNA biogenesis genes (RNASEN, DGCR8, XPO5, RAN) in K562 cell line (Table 3). [score:27]
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[+] score: 21
Notably, miR-122, miR-194, miRNA-101b, and miRNA-705 were upregulated and miRNA-376a, miRNA-127, miRNA-34a, miRNA-300 and miRNA-342-3p were downregulated in the liver tissue of MCD-fed mice treated with or without metformin (Table IB and Fig. 6). [score:7]
Of a number of upregulated miRNAs, miRNA-376a, miR-127, miR-34a, miR-300, miR-342-3p were downregulated following metformin treatment in MCD-fed mice. [score:7]
The five downregulated miRNAs i. e., miRNA-376a, miRNA-127, miRNA-34a, miRNA-300 and miRNA-342-3p, were identical to five of the 71 upregulated miRNAs in control and MCD-fed mice. [score:7]
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[+] score: 20
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-16-1, hsa-mir-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-20a, hsa-mir-21, hsa-mir-23a, hsa-mir-25, hsa-mir-26a-1, hsa-mir-27a, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-33a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-93, hsa-mir-96, hsa-mir-99a, hsa-mir-100, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-16-2, hsa-mir-198, hsa-mir-199a-1, hsa-mir-148a, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-10a, hsa-mir-10b, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-182, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-203a, hsa-mir-204, hsa-mir-210, hsa-mir-212, hsa-mir-181a-1, hsa-mir-214, hsa-mir-215, hsa-mir-216a, hsa-mir-217, hsa-mir-218-1, hsa-mir-218-2, hsa-mir-219a-1, hsa-mir-221, hsa-mir-222, hsa-mir-223, hsa-mir-224, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-27b, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-125b-1, hsa-mir-128-1, hsa-mir-130a, hsa-mir-132, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-142, hsa-mir-145, hsa-mir-191, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-134, hsa-mir-146a, hsa-mir-150, hsa-mir-186, hsa-mir-188, hsa-mir-193a, hsa-mir-194-1, hsa-mir-320a, hsa-mir-155, hsa-mir-181b-2, hsa-mir-128-2, hsa-mir-194-2, hsa-mir-106b, hsa-mir-29c, hsa-mir-219a-2, hsa-mir-34b, hsa-mir-34c, hsa-mir-99b, hsa-mir-130b, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-362, hsa-mir-369, hsa-mir-375, hsa-mir-378a, hsa-mir-382, hsa-mir-340, hsa-mir-328, hsa-mir-151a, hsa-mir-148b, hsa-mir-331, hsa-mir-339, hsa-mir-335, hsa-mir-345, hsa-mir-196b, hsa-mir-424, hsa-mir-425, hsa-mir-20b, hsa-mir-451a, hsa-mir-409, hsa-mir-484, hsa-mir-486-1, hsa-mir-487a, hsa-mir-511, hsa-mir-146b, hsa-mir-496, hsa-mir-181d, hsa-mir-523, hsa-mir-518d, hsa-mir-499a, hsa-mir-501, hsa-mir-532, hsa-mir-487b, hsa-mir-551a, hsa-mir-92b, hsa-mir-572, hsa-mir-580, hsa-mir-550a-1, hsa-mir-550a-2, hsa-mir-590, hsa-mir-599, hsa-mir-612, hsa-mir-624, hsa-mir-625, hsa-mir-627, hsa-mir-629, hsa-mir-33b, hsa-mir-633, hsa-mir-638, hsa-mir-644a, hsa-mir-650, hsa-mir-548d-1, hsa-mir-449b, hsa-mir-550a-3, hsa-mir-151b, hsa-mir-320b-1, hsa-mir-320c-1, hsa-mir-454, hsa-mir-320b-2, hsa-mir-378d-2, hsa-mir-708, hsa-mir-216b, hsa-mir-1290, hsa-mir-320d-1, hsa-mir-320c-2, hsa-mir-320d-2, hsa-mir-378b, hsa-mir-3151, hsa-mir-320e, hsa-mir-378c, hsa-mir-550b-1, hsa-mir-550b-2, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, hsa-mir-219b, hsa-mir-203b, hsa-mir-451b, hsa-mir-499b, hsa-mir-378j, hsa-mir-486-2
Using TaqMan miRNA microarray and quantitative real-time RT-PCR, Fayyad-Kazan found that the expression of let-7d, miR-150, miR-339, and miR-342 was down-regulated, and let-7b, and miR-523 was up-regulated in AML patient plasma compared to normal controls. [score:8]
When globally analyzed the relapse-related miRNAs-miR-7, miR-100, miR-216 and let-7i—were up-regulated, and miR-486, miR-191, miR-150, miR-487 and miR-342 were down-regulated in early relapse ALL patients [76]. [score:7]
Up-regulation of miR-150 and miR-342 after treatment was associated with AML patients with complete remission [164]. [score:4]
Analyses of over 430 miRNAs in 50 clinical T-ALL samples revealed a common signature: miR-223, miR-19b, miR-20a, miR-92, miR-142-3p, miR-150, miR-93, miR-26a, miR-16 and miR-342 [59]. [score:1]
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Reexpression of miR-342 may present a therapeutic approach in suppressing the growth of tamoxifen resistant breast cancer cells. [score:5]
Furthermore, the study also showed that miR-342 regulates gene expression in regards to tamoxifen -mediated apoptosis and proliferation. [score:4]
The miR-342 is downregulated in tamoxifen resistant breast cancer cell lines as well as in tamoxifen refractory breast cancers. [score:4]
The miR-342 was revealed to contribute to tamoxifen resistance in several mo dels, including cell lines that overexpress HER2Δ16 [85]. [score:3]
The miR-342 was revealed to play a tumor suppressive role in regards to tamoxifen resistant breast cancer. [score:3]
3.8. miRNA-342. [score:1]
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[+] score: 19
Other miRNAs from this paper: hsa-let-7b, hsa-mir-21, hsa-mir-27a, hsa-mir-148a, hsa-mir-10a, hsa-mir-10b, hsa-mir-34a, hsa-mir-203a, hsa-mir-1-2, hsa-mir-23b, hsa-mir-122, hsa-mir-141, hsa-mir-126, hsa-mir-146a, hsa-mir-1-1, hsa-mir-155, hsa-mir-34b, hsa-mir-34c, hsa-mir-296, hsa-mir-370, hsa-mir-373, hsa-mir-526a-1, hsa-mir-526a-2, hsa-mir-548a-1, hsa-mir-548b, hsa-mir-548a-2, hsa-mir-548a-3, hsa-mir-548c, hsa-mir-548d-1, hsa-mir-548d-2, hsa-mir-542, hsa-mir-548e, hsa-mir-548j, hsa-mir-548k, hsa-mir-548l, hsa-mir-548f-1, hsa-mir-548f-2, hsa-mir-548f-3, hsa-mir-548f-4, hsa-mir-548f-5, hsa-mir-1246, hsa-mir-548g, hsa-mir-548n, hsa-mir-548m, hsa-mir-548o, hsa-mir-548h-1, hsa-mir-548h-2, hsa-mir-548h-3, hsa-mir-548h-4, hsa-mir-548p, hsa-mir-548i-1, hsa-mir-548i-2, hsa-mir-548i-3, hsa-mir-548i-4, hsa-mir-548q, hsa-mir-548s, hsa-mir-466, hsa-mir-548t, hsa-mir-548u, hsa-mir-548v, hsa-mir-548w, hsa-mir-548x, hsa-mir-548y, hsa-mir-548z, hsa-mir-548aa-1, hsa-mir-548aa-2, hsa-mir-548o-2, hsa-mir-548h-5, hsa-mir-548ab, hsa-mir-548ac, hsa-mir-548ad, hsa-mir-548ae-1, hsa-mir-548ae-2, hsa-mir-548ag-1, hsa-mir-548ag-2, hsa-mir-548ah, hsa-mir-548ai, hsa-mir-548aj-1, hsa-mir-548aj-2, hsa-mir-548x-2, hsa-mir-548ak, hsa-mir-548al, hsa-mir-548am, hsa-mir-548an, hsa-mir-203b, hsa-mir-548ao, hsa-mir-548ap, hsa-mir-548aq, hsa-mir-548ar, hsa-mir-548as, hsa-mir-548at, hsa-mir-548au, hsa-mir-548av, hsa-mir-548aw, hsa-mir-548ax, hsa-mir-548ay, hsa-mir-548az, hsa-mir-548ba, hsa-mir-548bb, hsa-mir-548bc
Wang and the coworkers discovered that miR-342-5p could significantly inhibit CVB3 replication by directly targeting the 2C-coding region of the viral genome (Figure 2) [99]. [score:6]
The ectopic expression of miR-342-5p, miR-373 or miR-542-5p suppresses Enterovirus replication, but miR-10* facilitates CVB3 replication. [score:5]
Wang L. Qin Y. Tong L. Wu S. Wang Q. Jiao Q. Guo Z. Lin L. Wang R. Zhao W. MiR-342-5p suppresses coxsackievirus B3 biosynthesis by targeting the 2C-coding region Antivir. [score:4]
MiR-342-5p targets the CVB3 2C-coding region and thus inhibits CVB3 replication. [score:4]
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[+] score: 17
Emerging evidence demonstrates that miRNAs are critical regulators of lipid synthesis and FAO [81] resulting in defective cell metabolism and carcinogenesis [82] directly targeting key enzymes or transcription factors as oncogenes and tumor suppressors [81] as shown in Table  1. Table 1 miRNAs involved in cancer metabolic plasticity MiRNAs Target Reference miR-122 Cholesterol biosynthesis 88– 90 miR-370 Fatty acid oxidation, CPT1A [91] miR-378/378* Lipid metabolism, CrAT 92, 93 miR-335 Lipid metabolism and adipogenesis [94] miR-205 Lipid metabolism [95] miR-143 Adipocyte differentiation [96] miR-27 Adipolysis [97] miR-33a/b Cholesterol efflux and β-oxidation 98– 100 miR-185 Lipogenesis and cholesterogenesis [101] miR-342 Lipogenesis and cholesterogenesis [101] miR-124 CPT1A [27] miR-129 CACT 27, 102 MiR-122 was the first miRNA identified as tissue-specific, and it is the most abundant in liver involved in lipid metabolic reprogramming [83]. [score:9]
Furthermore, in prostate cancer cells, miR-185 and miR-342 control lipogenesis and cholesterogenesis by reducing the expression of SREBP-1/2 and downregulating their targeted genes, including fatty acid synthase [96]. [score:8]
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[+] score: 17
miRNA Tissue type Mode of action Reference miR-491-5p Cervical cancerUnknown, inhibits hTERT Zhao et al., 2015 miR-1182 Gastric cancerBinds the ORF of hTERT mRNA, preventing translation Zhang et al., 2015 miR-1207-5p Gastric cancerRepresses hTERT in normal tissues Chen et al., 2014 miR-1266 Gastric cancerRepresses hTERT in normal tissues Chen et al., 2014 miR-138 Anaplastic thyroid carcinoma (ATC)Interaction with 3′UTR of hTERT to reduce protein expression Mitomo et al., 2008 let-7g Pulmonary fibrosisInteraction with 3′UTR of hTERT to reduce expression Singh et al., 2010 miR-133a Jurkat cellsInteraction with 3′UTR of hTERT to reduce expression Hrdličková et al., 2014 miR-342 Jurkat cellsInteraction with the 3′UTR of hTERT to reduce expression Hrdličková et al., 2014 miR-541 Jurkat cellsInteraction with the 3′UTR of hTERT to reduce expression Hrdličková et al., 2014 Non-coding RNAs can also target transcription factors involved in the control of hTERT. [score:17]
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Using 15 down-regulated miRNAs (let-7 g, miR-101, miR-133a, miR-150, miR-15a, miR-16, miR-29b, miR-29c, miR-30a, miR-30b, miR-30c, miR-30d, miR-30e, miR-34b and miR-342), known to be associated with cancer, we found 16.5% and 11.0% of our PLS-predicted miRNA-targets, on average, were also predicted as targets for the corresponding miRNAs by TargetScan5.1 and miRanda, respectively (Table 2). [score:10]
With the aid of IPA pathway designer, we found that 27 of the 31 down-regulated miRNAs were linked to one or more mRNA networks and 20 of them (let-7 g, miR-101, miR-126, miR-133a, miR-142-5p, miR-150, miR-15a, miR-26b, miR-28, miR-29b, miR-30a, miR-30b, miR-30c, miR-30d, miR-30e, miR-34b, miR-99a, mmu-miR-151, mmu-miR-342 and rno-miR-151) were involved in all of the top 4 networks. [score:4]
We found that all 15 miRNAs were involved in cancer and tumorigenesis, 12 of them (all except miR-101, miR-15a and miR-29c) were in carcinoma, malignant tumor and primary tumor and 8 of them (all except let-7 g, miR-101, miR-150, miR-15a, miR-16, miR-29c and miR-342) were in angiogenesis as were shown in the last column of Table 5. Furthermore, we examined which associated miRNAs among the 15 cancer-related miRNAs were involved in the canonical pathways associated with cancer. [score:1]
We found that all 15 miRNAs were involved in cancer and tumorigenesis, 12 of them (all except miR-101, miR-15a and miR-29c) were in carcinoma, malignant tumor and primary tumor and 8 of them (all except let-7 g, miR-101, miR-150, miR-15a, miR-16, miR-29c and miR-342) were in angiogenesis as were shown in the last column of Table 5. Furthermore, we examined which associated miRNAs among the 15 cancer-related miRNAs were involved in the canonical pathways associated with cancer. [score:1]
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The other five miRNAs common on the three mo dels (miR-21a-5p, miR-125a-5p, miR-142a-3p, miR-146b-5p, and miR-342-3p) also have important immunological activities (Table 1) that would together favor antibody production and development of the murine disease. [score:4]
They were validated, together with the downregulated miR-342-3p, due to its previously reported importance in LES [14, 15]. [score:4]
These four miRNAs were chosen among the six detected as important in the lupus-like mo del by miRNA arrays, together with miR-342-3p [14, 15], because they were the only found in the compendium database of experimentally determined miRNA target genes created by the Cancer miRNA Regulatory Network [19]. [score:4]
It can be observed that the twelve deregulated miRNAs, together with miR-342-3p, found in the three-murine lupus-like mo dels, greatly impact the immune system. [score:2]
Additionally, miR-342-3p was added because of its importance in human lupus [14, 15], and RNU6 as an endogenous control. [score:1]
When deciding to validate only the six miRNAs found to be affected in all lupus-like mo dels tested, we added another miRNA, miR-342-3p, as this miRNA has previously been reported as important in human lupus [14, 15]. [score:1]
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For example, over expression of miR-127, a Dlk1-Dio3 mat NAFLD candidate, in pancreas islet cells suppresses insulin secretion and causes glucose intolerance [51]; additionally, miR-342 and miR-379 are upregulated in white adipose tissue of obese mice [52]. [score:8]
The miR-342 gene is located in 14q23.2, but not in the Dlk1-Dio3 mat region [30], and miR-342 expression is coupled to the host gene Ena/Vasp-like protein [48]. [score:3]
Indeed, the miR-342 expression pattern differed from those of the Dlk1-Dio3 mat candidate miRNAs. [score:3]
Further studies will be needed to clarify the function of miR-218 and miR-342 in NAFLD pathology. [score:1]
miR-218 and miR-342 were also newly predicted candidate NAFLD miRNAs based on mouse mo dels. [score:1]
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A gene expression profile revealed 140 altered mRNAs, from which 35 are potential direct targets of miR-342-3p defined by an in-silico analysis. [score:6]
Results We found low expression levels of miR-342-3p in TNBC tumors compared with other breast cancer phenotypes, and this down-regulation characterizes one of our miRNA subgroups with high risk to relapse. [score:3]
Results We found low expression levels of miR-342-3p in TNBC tumors compared with other breast cancer phenotypes, and this down-regulation characterizes one of our miRNA subgroups with high risk to relapse. [score:3]
The monocarboxylate transporter 1(MCT1), was confirmed as one target of miR-342-3p by a luciferase assay and western blot analysis. [score:2]
O11 A microRNA signature identifies subtypes of triple -negative breast cancer and reveals MIR-342-3P as regulator of a lactate metabolic pathway. [score:2]
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To determine whether miRNA dysfunction is involved in prion disease pathogenesis, the authors used a BSE-infected cynomolgus macaque mo del to confirm that miR-342-3p was upregulated in brain (152). [score:6]
2013.05.018 152 Montag J Hitt R Opitz L Schulz-Schaeffer WJ Hunsmann G Motzkus D. Upregulation of miRNA hsa-miR-342-3p in experimental and idiopathic prion disease. [score:6]
Moreover, the authors confirmed that hsa-miR-342-3p was upregulated in brain samples of human type 1 and type 2 sporadic CJD, suggesting that miR-342-3p may be a biomarker of prionopathies in animals and humans. [score:4]
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In contrast, the most down-regulated miRNAs, miR-342-3p and miR-26b, showed a prevalence of positive correlations with their targets (respectively 8/9 and 20/22), which indicate a more complex and possible indirect relationship with the regulated genes. [score:8]
When Sa/CD99 cells are terminally differentiated (day 14) [28], we observed a modulation of a different set of miRs: miR-342-3p was the most down-regulated, while miR-139-3p, miR-1288 and miR-1914* were the most up-regulated. [score:7]
Among the remaining 4 miRs (miR-26b, miR-34a, miR-342-3p, miR-520e), attention still points to miR-34a, which has the highest number (24) of predicted and correlated genes. [score:1]
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Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-mir-21, hsa-mir-26a-1, hsa-mir-27a, hsa-mir-28, hsa-mir-30a, hsa-mir-96, hsa-mir-98, hsa-mir-99a, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-196a-1, hsa-mir-199a-1, hsa-mir-148a, hsa-mir-30d, hsa-mir-34a, hsa-mir-196a-2, hsa-mir-199a-2, hsa-mir-23b, hsa-mir-27b, hsa-mir-125b-1, hsa-mir-143, hsa-mir-145, hsa-mir-152, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-194-1, hsa-mir-194-2, hsa-mir-200a, hsa-mir-99b, hsa-mir-26a-2, hsa-mir-378a, hsa-mir-148b, hsa-mir-338, hsa-mir-335, hsa-mir-196b, hsa-mir-484, hsa-mir-486-1, hsa-mir-1271, hsa-mir-378d-2, bta-mir-26a-2, bta-mir-103-1, bta-mir-148a, bta-mir-21, bta-mir-27a, bta-mir-30d, bta-mir-484, bta-mir-99a, bta-mir-125a, bta-mir-125b-1, bta-mir-145, bta-mir-199a-1, bta-mir-27b, bta-mir-98, bta-mir-148b, bta-mir-200a, bta-mir-30a, bta-let-7a-1, bta-mir-342, bta-mir-23b, bta-let-7a-2, bta-let-7a-3, bta-mir-103-2, bta-mir-125b-2, bta-mir-34a, bta-mir-99b, hsa-mir-885, hsa-mir-103b-1, hsa-mir-103b-2, bta-mir-143, bta-mir-152, bta-mir-16a, bta-mir-194-2, bta-mir-196a-2, bta-mir-196a-1, bta-mir-196b, bta-mir-199a-2, bta-mir-26a-1, bta-mir-28, bta-mir-335, bta-mir-338, bta-mir-378-1, bta-mir-486, bta-mir-885, bta-mir-96, bta-mir-1271, bta-mir-2299, bta-mir-199c, bta-mir-1388, bta-mir-194-1, bta-mir-378-2, hsa-mir-378b, bta-mir-3431, hsa-mir-378c, hsa-mir-4286, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, bta-mir-4286-1, bta-mir-4286-2, hsa-mir-378j, bta-mir-378b, bta-mir-378c, hsa-mir-486-2, bta-mir-378d, bta-mir-194b, bta-mir-194b-2
miR-342 can inhibit the expression of SREBP, resulting in down-regulation of FASN and 3-hydroxy-3-methylglutaryl CoA reductase (HMGCR) and inhibition of FA biosynthesis in prostate cancer cells [75]. [score:10]
When compared with the control period (day-14), we identified a total of 22 DE miRNAs at day+28 including 10 up-regulated (bta-miR-199c, miR-199a-3p, miR-98, miR-378, miR-21-5p, miR-148b, miR-34a, miR-152, miR-16a, and miR-28) and 12 down-regulated (bta-miR-200a, miR-145, miR-99a-5p, miR-125b, miR-99b, miR-125a, miR-96, miR-484, miR-1388-5p, miR-342, miR-486 and miR-1271) (Table  2). [score:6]
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[+] score: 16
miR-342 was found to be downregulated in CRC cells, and restoration of its expression downregulated DNMT1 and reactivated expression of cancer-related genes through demethylation of their promoter regions (Wang et al., 2011a). [score:11]
MicroRNA-342 inhibits colorectal cancer cell proliferation and invasion by directly targeting DNA methyltransferase 1. Carcinogenesis 32 1033– 1042 10.1093/carcin/bgr081 21565830 Wang Z. Chen Z. Gao Y. Li N. Li B. Tan F. (2011b). [score:5]
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In the MCF-7 cell line over -expression of miR-342 leads to reduced proliferation, which is in line with its low expression in TP53 mutated samples. [score:5]
At top among the 81 differentially expressed miRNAs (at 5% FDR) we identified miR-342-3p (TNoM p < 2E-08) to have significantly lower expression in the TP53 mutant tumors. [score:5]
The let-7 family and miR-342 exhibit, in our cohort, a more significant differential expression between TP53 mutational statuses than between ER statuses or tumor subtypes. [score:4]
CAN-0007-1585 39 Grady WM Parkin RK Mitchell PS Lee JH Kim YH 2008 Epigenetic silencing of the intronic microRNA hsa-miR-342 and its host gene EVL in colorectal cancer. [score:1]
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For example, miR-129-5p induces interferon-β which down-regulates E6 and E7 expression [19], miR-26a and miR-342-3p inhibit cell proliferation and invasion through each protein tyrosine phosphatase type IVA 1 and the mitogen-activated protein kinase (MAPK) pathway or forkhead box M1 [20, 21], and miR-101 regulates the cell cycle by inhibiting the G1-to-S transition [22]. [score:11]
Li X. Chu H. Lv T. Wang L. Kong S. Dai S. MiR-342–3p suppresses proliferation, migration and invasion by targeting FOXM1 in human cervical cancer FEBS Lett. [score:4]
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Upregulation of miRNA-146a-5p in the neocortex of sCJD cases (n = 3 sCJD, n = 3 controls) [65] and upregulation of miRNA-342-3p in sCJD brain tissue (n = 2 sCJD, n = 1 control) [23] are in agreement with our observations. [score:7]
Six miRNAs were selected: i) miRNA-195-5p, 877-5p and 323a-5p, commonly regulated in the FC of sCJD and in the PFC of AD, ii) miRNA-146a-5p and miRNA-342-3p, reported to be altered in AD and prion disease mo dels [22, 23, 53, 54] and iii) miRNA-5701. [score:4]
Additionally, two miRNAs upregulated in the basis pontis of bovine spongiform encephalopathy-infected macaques, miRNA-342-3p and miRNA-494-3p [23], were also enriched in sCJD, but exclusively in the FC region. [score:4]
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[+] score: 15
The predicted and experimentally proven targets of each miRNA that reduced proliferation provided by the IPA program are shown in Table 2. In total, 6,458 target genes were predicted by the IPA program for the eight miRNAs that reduced proliferation found in our study available in IPA, ranging from 448 genes for miR-342-5p to 2,149 genes for the miR-129 cluster. [score:5]
miRNA Expressionp-value Expression fold change (log2) Survivalp-value hsa-miR-136 7.52E-14 −1.69 NS hsa-miR-145 5.88E-04 −1.04 0.005 hsa-miR-155 1.18E-21 1.94 NS hsa-miR-181b 5.44E-02 −0.22 NS hsa-miR-342 4.35E-10 −1.25 NS hsa-miR-129 1.29E-16 −3.39 NS hsa-miR-376a 4.35E-07 −0.63 NS hsa-miR-376b 7.37E-02 0.07 NS Survival p-value was calculated from miRNA expression data with Kaplan-Meier analysis. [score:5]
MiR-342 is an important mediator of tamoxifen response in breast tumor cell lines and breast cancer patients; restoring miR-342 expression sensitized breast cancer cells to tamoxifen -induced apoptosis with a dramatic reduction in cell growth [26]. [score:3]
MiR-342-5p is predicted to target EIF2AK1, which we found was a proliferation-reducing hit when silenced in the GBM cell lines. [score:2]
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[+] score: 14
In particular, these studies identified miR15/miR-16, miR-26, miR-29, miR-107, miR-142, miR-342, and let7 between the miRNAs significantly induced, whereas miR-181b was found to be downregulated by ATRA. [score:4]
The PML/RAR α  oncogenic fusion protein is directly responsible for the silencing of the tumor suppressors let-7c and miR-342. [score:4]
Ectopic expression for some of these miRNAs, such as miR-26a, miR-29a, miR-142-3p and miR-342, has been produced and, similarly to miR-223, it stimulated granulocytic differentiation of AML cells [38, 41, 43, 44]. [score:3]
1 also controls the expression of miR-146a, miR-342, miR-338, and miR-155 during monocytopoiesis of mouse myeloid progenitor cell lines [58]. [score:3]
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[+] score: 14
We also identified miR-342-3p to be upregulated in RRMS patients; a miRNA especially enriched in microglia and dysregulated in Creutzfeldt-Jakob and Alzheimer’s disease 33– 35. [score:7]
Differential expression analysis between the validation group and RRMS samples identified eight out of nine significantly dysregulated miRNAs as identified previously (miR-15b-5p, miR-23a-3p, miR-223-3p, miR-374a-5p, miR-30b-5p, miR-433-3p, miR-485-3p, miR-342-3p, miR-432-5p) (Table  3). [score:4]
Both miR-342-3p and mir-30b-5p have been proposed as free circulating miRNA biomarkers in Alzheimer’s and Parkinson’s diseases 27, 28, and their association with MS in this study suggests that they may be more general markers of neuro-axonal injury. [score:3]
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[+] score: 14
Differential expression of RNAseq data identified 12 miR with changes in relative expression during follicular trachoma, of which 9 were confirmed as differentially expressed by qPCR (miR-155, miR-150, miR-142, miR-181b, miR-181a, miR-342, miR-132, miR-4728 and miR-184). [score:7]
are shown in Table  2. MiR-155, miR-150, miR-142, miR-181b, miR-181a and miR-342 were up-regulated in all 3 comparisons (Fig.   2). [score:4]
MiR-155, miR-150, miR-142, miR-181b, miR-181a, miR-342 and miR-132 were differentially expressed during current Ct infection. [score:3]
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[+] score: 12
Twelve radiation -suppressed miRNAs were identified, i. e. let-7d, miR-15a, miR-17, miR-30d, miR-92a, miR-197, miR-221, miR-320b, miR-342, miR-361, miR-501 and miR-671, and a significantly different expression between prostate cancer and the corresponding adjacent part was found, including 11 upregulated and 1 downregulated (Fig. 3B). [score:11]
In the present study, we also identified radiation-response miRNAs that had been reported in other types of cancer but not in prostate cancer, such as miR-25, miR-15a, miR-30d, miR-125a, miR-221 and miR-342 (21, 56– 63). [score:1]
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miRNA target has-miR302a MECP2 hsa-miR29a TET1, TET2, TET3 has-miR29a/c DNMT3A, DNMT3B has-miR29b-1/2 DNMT1 (Indirect via SP1) hsa-miR148a DNMT3B hsa-miR148a DNMT1 hsa-miR152 DNMT1 has-miR302a DNMT1 (Indirect via AOF2) hsa-miR342 DNMT1 hsa-miR17-92 DNMT1 hsa-miR26a-1/2 EZH2 hsa-miR101-1/2 EZH2/EED hsa-miR214 EZH2 hsa-miR128-1/2 BMI-1 hsa-miR199a-1/2 BRM hsa-miR433 HDAC6 hsa-miR449a HDAC1 hsa-miR138 SIRT1In the first column we report a list of miRNAs which are known to target epigenetic regulators and in the second column the corresponding targets. [score:10]
It is well known (see for instance Gruber and Zavolan, 2013) that Dnmt proteins are strictly controlled in a coordinated way by a number of miRNAs, among them in particular mir-29a/b/c, mir-152, mir148a, mir342, mir302 and various members of the cluster mir17-92. [score:1]
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In the case of miR-342 –miR-93 one may presume that before sponging, this edge was not present because of the lower reaction rates between these two miRNAs and the common target compared to the significantly higher reaction rate between the miRNAs of group S with this specific target. [score:4]
After sponging, despite the lower reaction rates, the target becomes more available for miR-342 and miR-93, thus increasing their competition over it. [score:3]
This was reflected by the appearance of a new edge between miR-342 and miR-93 (red line in Fig 4). [score:1]
Also, we observed that only two new edges appear (red edges), an edge that connects miR-342 with miR-93 and an edge that connects miR-16 with miR-486. [score:1]
New edges appear between miR-93 and miR-342 and between miR-16 and miR-486. [score:1]
In both, control and septic patient network, the same miRNAs remain very well connected (miR-21, miR-223 and miR-342). [score:1]
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Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-16-1, hsa-mir-21, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-26a-1, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-99a, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-16-2, hsa-mir-192, hsa-mir-148a, hsa-mir-10b, hsa-mir-181a-2, hsa-mir-181a-1, hsa-mir-215, hsa-mir-223, hsa-mir-224, hsa-mir-200b, hsa-mir-15b, hsa-mir-27b, hsa-mir-125b-1, hsa-mir-141, hsa-mir-143, hsa-mir-152, hsa-mir-125b-2, hsa-mir-126, hsa-mir-146a, hsa-mir-184, hsa-mir-200c, hsa-mir-155, hsa-mir-29c, hsa-mir-200a, hsa-mir-99b, hsa-mir-296, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-378a, hsa-mir-148b, hsa-mir-451a, ssc-mir-125b-2, ssc-mir-148a, ssc-mir-15b, ssc-mir-184, ssc-mir-224, ssc-mir-23a, ssc-mir-24-1, ssc-mir-26a, ssc-mir-29b-1, ssc-let-7f-1, ssc-mir-103-1, ssc-mir-21, ssc-mir-29c, hsa-mir-486-1, hsa-mir-499a, hsa-mir-671, hsa-mir-378d-2, bta-mir-26a-2, bta-mir-29a, bta-let-7f-2, bta-mir-103-1, bta-mir-148a, bta-mir-16b, bta-mir-21, bta-mir-499, bta-mir-99a, bta-mir-125b-1, bta-mir-126, bta-mir-181a-2, bta-mir-27b, bta-mir-31, bta-mir-15b, bta-mir-215, bta-mir-30e, bta-mir-148b, bta-mir-192, bta-mir-200a, bta-mir-200c, bta-mir-23a, bta-mir-29b-2, bta-mir-29c, bta-mir-10b, bta-mir-24-2, bta-mir-30a, bta-mir-200b, bta-let-7a-1, bta-mir-342, bta-let-7f-1, bta-let-7a-2, bta-let-7a-3, bta-mir-103-2, bta-mir-125b-2, bta-mir-15a, bta-mir-99b, hsa-mir-664a, ssc-mir-99b, hsa-mir-103b-1, hsa-mir-103b-2, ssc-mir-15a, ssc-mir-16-2, ssc-mir-16-1, bta-mir-141, bta-mir-143, bta-mir-146a, bta-mir-152, bta-mir-155, bta-mir-16a, bta-mir-184, bta-mir-24-1, bta-mir-223, bta-mir-224, bta-mir-26a-1, bta-mir-296, bta-mir-29d, bta-mir-378-1, bta-mir-451, bta-mir-486, bta-mir-671, bta-mir-29e, bta-mir-29b-1, bta-mir-181a-1, ssc-mir-181a-1, ssc-mir-215, ssc-mir-30a, bta-mir-2318, bta-mir-2339, bta-mir-2430, bta-mir-664a, bta-mir-378-2, ssc-let-7a-1, ssc-mir-378-1, ssc-mir-29a, ssc-mir-30e, ssc-mir-499, ssc-mir-143, ssc-mir-10b, ssc-mir-486-1, ssc-mir-152, ssc-mir-103-2, ssc-mir-181a-2, ssc-mir-27b, ssc-mir-24-2, ssc-mir-99a, ssc-mir-148b, ssc-mir-664, ssc-mir-192, ssc-mir-342, ssc-mir-125b-1, oar-mir-21, oar-mir-29a, oar-mir-125b, oar-mir-181a-1, hsa-mir-378b, hsa-mir-378c, ssc-mir-296, ssc-mir-155, ssc-mir-146a, bta-mir-148c, ssc-mir-126, ssc-mir-378-2, ssc-mir-451, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, hsa-mir-451b, hsa-mir-499b, ssc-let-7a-2, ssc-mir-486-2, hsa-mir-664b, hsa-mir-378j, ssc-let-7f-2, ssc-mir-29b-2, ssc-mir-31, ssc-mir-671, bta-mir-378b, bta-mir-378c, hsa-mir-486-2, oar-let-7a, oar-let-7f, oar-mir-103, oar-mir-10b, oar-mir-143, oar-mir-148a, oar-mir-152, oar-mir-16b, oar-mir-181a-2, oar-mir-200a, oar-mir-200b, oar-mir-200c, oar-mir-23a, oar-mir-26a, oar-mir-29b-1, oar-mir-30a, oar-mir-99a, bta-mir-664b, chi-let-7a, chi-let-7f, chi-mir-103, chi-mir-10b, chi-mir-125b, chi-mir-126, chi-mir-141, chi-mir-143, chi-mir-146a, chi-mir-148a, chi-mir-148b, chi-mir-155, chi-mir-15a, chi-mir-15b, chi-mir-16a, chi-mir-16b, chi-mir-184, chi-mir-192, chi-mir-200a, chi-mir-200b, chi-mir-200c, chi-mir-215, chi-mir-21, chi-mir-223, chi-mir-224, chi-mir-2318, chi-mir-23a, chi-mir-24, chi-mir-26a, chi-mir-27b, chi-mir-296, chi-mir-29a, chi-mir-29b, chi-mir-29c, chi-mir-30a, chi-mir-30e, chi-mir-342, chi-mir-378, chi-mir-451, chi-mir-499, chi-mir-671, chi-mir-99a, chi-mir-99b, bta-mir-378d, ssc-mir-378b, oar-mir-29b-2, ssc-mir-141, ssc-mir-200b, ssc-mir-223, bta-mir-148d
miRNA-342 was observed to inhibit colorectal cancer cell proliferation and invasion by directly targeting DNA methyltransferase 1 (Wang et al., 2011). [score:6]
MicroRNA-342 inhibits colorectal cancer cell proliferation and invasion by directly targeting DNA methyltransferase 1. Carcinogenesis 32 1033– 1042. [score:5]
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Also, miR-221 and miR-222 were upregulated while miR-21, miR-342, and miR-489 were downregulated in tamoxifen-resistant MCF-7 cells; the reintroduction of miR-221 or miR-222 rendered the parent MCF-7 cells resistance to tamoxifen through inhibiting their target p27Kip1, which was reduced by 50% in resistant cells [17]. [score:11]
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control Expression in case group 1 hsa-mir-1290 0.26 down 2 hsa-mir-342-5p 0.22 down 3 hsa-mir-1224-5p 0.23 down 4 hsa-mir-345 0.38 down 5 hsa-mir-1228 0.38 down 6 hsa-mir-1249 0.32 down 7 hsa-mir-1826 0.26 down 8 hsa-miR-1306 0.38 down 9 hsa-miR-188-5p 0.43 down 10 hsa-miR-320a 0.48 down 11 hsa-miR-320c 0.26 down 12 hsa-miR-365 0.31 down 13 hsa-miR-423-5p 0.35 down 14 hsa-miR-483-5p 0.25 down 15 hsa-miR-634 0.31 down 16 hsa-miR-671-5p 0.23 down 17 hsa-miR-939 0.24 down 18 hsa-miR-1246 2.22 up 19 hsa-miR-150 10.41 up 20 hsa-miR-574-5p 8.04 up Table 3 MiRNAs Target Gene Symbol hsa-miR-345PUM2, PPP2R3A, BCAT1, ZFHX4, CHSY3, ARNT, SHE, SLC7A5, SOS1,. [score:5]
control Expression in case group 1 hsa-mir-1290 0.26 down 2 hsa-mir-342-5p 0.22 down 3 hsa-mir-1224-5p 0.23 down 4 hsa-mir-345 0.38 down 5 hsa-mir-1228 0.38 down 6 hsa-mir-1249 0.32 down 7 hsa-mir-1826 0.26 down 8 hsa-miR-1306 0.38 down 9 hsa-miR-188-5p 0.43 down 10 hsa-miR-320a 0.48 down 11 hsa-miR-320c 0.26 down 12 hsa-miR-365 0.31 down 13 hsa-miR-423-5p 0.35 down 14 hsa-miR-483-5p 0.25 down 15 hsa-miR-634 0.31 down 16 hsa-miR-671-5p 0.23 down 17 hsa-miR-939 0.24 down 18 hsa-miR-1246 2.22 up 19 hsa-miR-150 10.41 up 20 hsa-miR-574-5p 8.04 up Table 3 MiRNAs Target Gene Symbol hsa-miR-345PUM2, PPP2R3A, BCAT1, ZFHX4, CHSY3, ARNT, SHE, SLC7A5, SOS1,. [score:5]
hsa-miR-342-5pAFF4, GSG1L, CACNB1, NPTXR, C1QTNF3, ITGA10, ATXN7L3, SLC7A5,. [score:1]
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[+] score: 10
With regard to miRNAs included in the “ECM & focal adhesion” node, miR-342 expression correlates with ER expression and tamoxifen sensitivity in breast tumors 22– 24. [score:5]
Moreover, miR-139-5p, miR-149, miR-449a and miR-342 were overexpressed in ER+ tumors with regard to TNBCs 10, 24, 48, 49. [score:3]
Both miR-149 and miR-342 have been included in a prognostic signature for breast cancer [25]. [score:1]
The “ECM & focal adhesion” node showed higher activity in ER-true tumors, and includes miR-139-5p, miR-149, miR-766, miR-342, miR-214* and miR-31. [score:1]
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Similar analysis in mouse metastatic sarcomas revealed overlap for several downregulated miRNAs including miR-16, miR-103, miR-146a, miR-223, miR-342 and miR-511. [score:4]
By comparing the downregulated miRNAs in metastatic sarcomas from human and mouse, we found six miRNAs common to both: miR-16, miR-103, miR-146a, miR-223, miR-342 and miR-511 (Fig.  1D,E). [score:4]
Cells overexpressing miR-146a and miR-342 showed a decrease only in the invasion assay, not in migration. [score:2]
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They found that upregulation of miR-499a-5p is a common feature of all placental insufficiencies such as preeclampsia (n = 80), gestational hypertension (n = 35), and FGR (n = 35); in addition, they demonstrated an upregulation of miR-1-3p in FGR pregnancies with abnormal umbilical fetal flows (n = 19); finally, they found downregulation of a series of miRNAs (miR-16-5p, miR-26a-5p, miR-100-5p, miR-103a-3p, miR-122-5p, miR-125b-5p, miR-126-3p, miR-143-3p, miR-145-5p, miR-195-5p, miR-199a-5p, miR-221-3p, miR-342-3p, and miR-574-3p) in FGR requiring the delivery before 34 weeks of gestation. [score:10]
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Other miRNAs from this paper: hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-16-1, hsa-mir-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-20a, hsa-mir-21, hsa-mir-22, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-93, hsa-mir-98, hsa-mir-99a, hsa-mir-100, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-106a, hsa-mir-16-2, hsa-mir-196a-1, hsa-mir-199a-1, hsa-mir-148a, hsa-mir-30c-2, hsa-mir-30d, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-10a, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-196a-2, hsa-mir-199a-2, hsa-mir-210, hsa-mir-181a-1, hsa-mir-214, hsa-mir-222, hsa-mir-223, hsa-mir-27b, hsa-mir-30b, hsa-mir-122, hsa-mir-125b-1, hsa-mir-130a, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-140, hsa-mir-141, hsa-mir-142, hsa-mir-143, hsa-mir-145, hsa-mir-191, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-127, hsa-mir-146a, hsa-mir-150, hsa-mir-186, hsa-mir-188, hsa-mir-195, hsa-mir-200c, hsa-mir-155, hsa-mir-181b-2, hsa-mir-106b, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-34b, hsa-mir-34c, hsa-mir-301a, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-363, hsa-mir-302c, hsa-mir-370, hsa-mir-373, hsa-mir-374a, hsa-mir-328, hsa-mir-326, hsa-mir-135b, hsa-mir-338, hsa-mir-335, hsa-mir-345, hsa-mir-424, hsa-mir-20b, hsa-mir-146b, hsa-mir-520a, hsa-mir-518a-1, hsa-mir-518a-2, hsa-mir-500a, hsa-mir-513a-1, hsa-mir-513a-2, hsa-mir-92b, hsa-mir-574, hsa-mir-614, hsa-mir-617, hsa-mir-630, hsa-mir-654, hsa-mir-374b, hsa-mir-301b, hsa-mir-1204, hsa-mir-513b, hsa-mir-513c, hsa-mir-500b, hsa-mir-374c
Ballabio et al. [59] also showed that direct targeting of EVL which is the host gene of miR-342, by the upregulated miRNA, miR-199a* was responsible for its downregulation. [score:10]
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51
[+] score: 10
In addition, hsa-miR-332-3p is thought to associate with idiopathic prion disease and it has been proposed that the upregulation of hsa-miR-342-3p may be a general phenomenon in late stage prion disease and might be used as a novel marker for animal and Human Transmissible Spongiform Encephalopathies (human TSEs) [45]. [score:8]
The utility of those 13 miRNAs, that is, hsa-miR-628-5p, hsa-miR-6804-3p, hsa-miR-4289, hsa-miR-208a-3p, hsa-miR-510-3p, hsa-miR-18a-3p, hsa-miR-329-3p, hsa-miR-548ax, hsa-miR-3934-5p, hsa-miR-4474-5p, hsa-miR-7974, hsa-miR-6865-5p, and hsa-miR-342-3p, can be utilized as antiviral therapeutics against MERS-CoV infection. [score:1]
Other hairpins MD5, MD17, MD157, MD244, MD366, MR175, MR201, MR268, and MR282 were aligned with hsa-miR-628-5p, hsa-miR-6804-3p, hsa-miR-4289, hsa-miR-208a-3p, hsa-miR-510-3p, hsa-miR-18a-3p, hsa-miR-329-3p, hsa-miR-548ax, and hsa-miR-342-3p, respectively. [score:1]
[1 to 20 of 3 sentences]
52
[+] score: 9
Dysregulated miRs in breast CAF included upregulation of miR-221, miR-31, and miR-221 with the downregulation of miR205, miR-200b, miR-200c, miR-141, miR-101, miR-342, let-7g and miR-26b affecting all aspects of cell differentiation and paracrine regulation (Zhao et al. 2012). [score:9]
[1 to 20 of 1 sentences]
53
[+] score: 9
Of the 186 miRNAs the expression of which was altered, nine were up-regulated at both time points (miR-125a-3p, miR-297c, miR-421, miR-452, miR-483, miR-574-3p, miR-574-5p, miR-669a, miR-720) and 11 were down-regulated at both time points (let-7g, miR-107, miR-10a, miR-15a, miR-15b, miR-199b*, miR-26a, miR-29c, miR-324-5p, miR-331-3p, miR-342-3p). [score:9]
[1 to 20 of 1 sentences]
54
[+] score: 9
Activated B cells and CLL cells exhibit similar miR expression profiles that include the upregulation of miR-34a, miR-155, and miR-342-3p and the downregulation of miR-103, miR-181a, and miR-181b [10]. [score:9]
[1 to 20 of 1 sentences]
55
[+] score: 9
Contrary to the high dose of 6 Gy where all the responding miRNAs are down-regulated in proliferating keratinocytes, the very low dose of 10 mGy leads to a particular response with only two up-regulated miRNAs: miR-342-3p and miR-708-5p. [score:7]
Further experiments will be necessary to precise how miR-342-3p and miR-708-5p might be involved in this particular response. [score:1]
It has been previously observed that genotoxic stresses, such as UV or IR, induce a very specific response in differentiated keratinocytes including induction of terminal differentiation [36, 37]: among the 12 miRNAs that we found induced after irradiation in differentiated keratinocytes, 5 of them (miR-125b-5p, let-7b-5p, miR-181a-5p, miR-195-5p and miR-342-3p) have been previously observed as being also induced during the differentiation process of human keratinocytes [38]. [score:1]
[1 to 20 of 3 sentences]
56
[+] score: 8
In breast cancer, 11 dysregulated miRNAs were identified in CAFs: 3 up-regulated miRNAs, miR-221-5p, miR-31-3p, and miR-221-3p, and 8 down-regulated miRNAs, miR-205, miR-00b, miR-200c, miR-141, miR-101, miR-342-3p, let-7 g, and miR-26b [16]. [score:8]
[1 to 20 of 1 sentences]
57
[+] score: 8
Modulation of pulmonary miRNAs targeting p53 (miR-138 and miR-376c) and apoptosis (miR-98 and miR-350) is consistent with the notion that AMPK is involved in the p53 -mediated cell cycle arrest and apoptosis 2. Several miRNAs upregulated in the lung of metformin -treated mice, including miR-30b, miR-138, miR-239a, miR-342, and miR-574, are involved in stress response and inflammation and target NF κB or Tlr9 (Toll-like receptor). [score:8]
[1 to 20 of 1 sentences]
58
[+] score: 8
Czimmerer et al. profiled miRNA expression in IL-4 -mediated activation and identified miR-342-3p, miR-99b, and miR-125a-5p as regulators of MΦ survival (83). [score:4]
These miRNAs are involved in IL-4/STAT6 signaling, with miR-342-3p directly targeting an anti-apoptotic network that includes BCL2L1. [score:4]
[1 to 20 of 2 sentences]
59
[+] score: 7
miR-342 12.3Upregulated after neurodegeneration [48] miR-21 12.1Upregulated after spinal cord injury [38]. [score:7]
[1 to 20 of 1 sentences]
60
[+] score: 7
Interestingly, miR-125b and miR-342-3p mimics increased the expression of MSI1 in HCT-116 and DLD-1 respectively, suggesting an alternative mechanism of MSI1 regulation. [score:4]
Although this observation is beyond the scope of our current study, future studies focused on the miR-125b and miR-342-3p regulation of MSI1 may be of interest. [score:2]
Among the three prediction programs, five overlapping miRNAs contained conserved, potential binding sites within MSI1 3′UTR; miR-125b, miR-137, miR-144, miR-185, and miR-342-3p (Figure 1B, Supplemental Table 1). [score:1]
[1 to 20 of 3 sentences]
61
[+] score: 7
Furthermore, re -expression of miR-320a [17], miR-375 [18], and miR-342 [19] could restore tamoxifen sensitivity by inhibiting their targets. [score:7]
[1 to 20 of 1 sentences]
62
[+] score: 7
However, Sp110 upregulated miR-155, miR-342, miR-3470a, miR-532 and miR-690. [score:4]
Of note, in both uninfected and Mtb-infected macrophages, Sp110 induced miR-155, miR-342, miR-3470a and miR-532, but inhibited let-7e, miR-1249, miR-125a, miR-132, miR-152, miR-16-1, miR-182, miR-183, miR-23a, miR-28a, miR-5114, miR-99a and miR-99b. [score:3]
[1 to 20 of 2 sentences]
63
[+] score: 7
Their results included two of the most upregulated (miR-221 and miR-222) and six downregulated miRNAs (miR-151-3p, miR-19a, miR-20b, miR-342-3p, miR-363, and miR-576-3p). [score:7]
[1 to 20 of 1 sentences]
64
[+] score: 7
In particular, miR-30c-1-3p was significantly upregulated and miR-181a-3p, miR-342-3p, and miR-450b-5p were significantly downregulated in ovarian cancer patients. [score:7]
[1 to 20 of 1 sentences]
65
[+] score: 7
Among miRNA analyzed, miR-23b, miR-30d, miR-132, miR-140-3p, miR-145, miR-150, miR-204 were up-regulated in OA chondrocytes whereas miR-22, miR-25, miR-26, miR-30c, miR-92b, miR-127, miR-194, miR-197, miR-296-5p, miR-342-3p, miR-488 were down-regulated in OA chondrocytes (Figure  1B). [score:7]
[1 to 20 of 1 sentences]
66
[+] score: 6
Additionally, let-7g*, miR-133a, miR-342-5p and miR-491-5p downregulate telomerase activity and inhibit cell proliferation [169]. [score:6]
[1 to 20 of 1 sentences]
67
[+] score: 6
Seven miRNAs (mmu-miR-574-5p, mmu-miR-466i-5p, mmu-miR-342-3p, mmu-let7i-5p, mmu-miR-34a-5p, mmu-miR-188-5p and mmu-miR-5119) were upregulated and the other five (mmu-miR-378a-3p, mmu-miR-202-3p, mmu-miR-378b, mmu-miR-378d and mmu-miR-212-3p) were downregulated in the CCl [4] group compared with the control (Fig. 1a,b). [score:6]
[1 to 20 of 1 sentences]
68
[+] score: 6
Compared to ALK(−) ALCLs, miR-203, miR-135b, miR-886-5p/3p, miR-20b, miR-106a and miR-183 were significantly upregulated in ALK(+) ALCLs while others (miR-155, miR-181a, miR-210, miR-29a/b, miR-342-5p/3p, miR-369-3p miR-374a/b, miR-423-5p, miR-625, miR-205, miR-146a and miR-26a) were down-regulated (Table 1). [score:6]
[1 to 20 of 1 sentences]
69
[+] score: 6
Reversely, tumor suppressor, including miR-222, miR-342-3p, were remarkably down-regulated in rpESCs. [score:6]
[1 to 20 of 1 sentences]
70
[+] score: 5
It is apparent that microRNAs can target genes/transcription factors that have a role at different stages of embryogenesis, for example miR-342 targets genes such as GATA-4, involved in the formation of definitive endoderm [41] and transcription factors FOXA2 and MAFB both involved in beta-cell differentiation and maturation [39, 42]. [score:5]
[1 to 20 of 1 sentences]
71
[+] score: 5
In another study, miR-342-3p is reported to suppress proliferation, migration and invasion by targeting FOXM1 in human cervical cancer [60]. [score:5]
[1 to 20 of 1 sentences]
72
[+] score: 5
Comparisons with computationally predicted RRM2 targeting miRNAs identified that in addition to reduction in several let-7 members, mir-140-3p, the miR-30 family, and miR-342-5p were also found to potentially contribute to the overall induction of RRM2 expression in Capan-1-GR cells (Fig. 4F ). [score:5]
[1 to 20 of 1 sentences]
73
[+] score: 5
In acute promyelocytic leukemia cells, IRF1 expression is associated with miR-342 [34]. [score:3]
1, interferon regulatory factor proteins and miR-342 stimulates ATRA -mediated granulocytic differentiation of acute promyelocytic leukemia cells. [score:2]
[1 to 20 of 2 sentences]
74
[+] score: 5
There were no detectable correlations between hsa-miR-451, hsa-miR-342-5p and their target genes, which may be due to the small quantity of target genes for these 2 miRNAs in database (Table 2). [score:5]
[1 to 20 of 1 sentences]
75
[+] score: 5
Thirty-three microRNAs in the array were found to be highly expressed (including let7a, miR-16, miR-21, and miR-205) and 22 showed low levels of expression (including miR-342, miR-346, and miR-373*) in all cell lines. [score:5]
[1 to 20 of 1 sentences]
76
[+] score: 5
CCR-15-2313 26957561 8. Weng W FOXM1 and FOXQ1 are promising prognostic biomarkers and novel targets of tumor-suppressive miR-342 in human colorectal cancerClin. [score:5]
[1 to 20 of 1 sentences]
77
[+] score: 5
MIMAT0000434 (hsa-miR-142) is reported to relate to the regulation of tumorigenicity of human breast cancer through the canonical WNT signaling pathway [30], and MIMAT0000753 (hsa-miR-342) regulates BRCA1 expression through modulation of ID4 in breast cancer [31]. [score:5]
[1 to 20 of 1 sentences]
78
[+] score: 4
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-16-1, hsa-mir-17, hsa-mir-18a, hsa-mir-19b-2, hsa-mir-20a, hsa-mir-21, hsa-mir-22, hsa-mir-26a-1, hsa-mir-29a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-93, hsa-mir-99a, hsa-mir-101-1, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-106a, hsa-mir-16-2, hsa-mir-197, hsa-mir-199a-1, hsa-mir-148a, hsa-mir-30c-2, hsa-mir-10a, hsa-mir-34a, hsa-mir-182, hsa-mir-199a-2, hsa-mir-205, hsa-mir-210, hsa-mir-221, hsa-mir-223, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-23b, hsa-mir-122, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-125b-1, hsa-mir-132, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-140, hsa-mir-142, hsa-mir-143, hsa-mir-125b-2, hsa-mir-134, hsa-mir-146a, hsa-mir-150, hsa-mir-206, hsa-mir-155, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-101-2, hsa-mir-130b, hsa-mir-26a-2, hsa-mir-361, hsa-mir-362, hsa-mir-363, hsa-mir-376c, hsa-mir-371a, hsa-mir-375, hsa-mir-376a-1, hsa-mir-378a, hsa-mir-151a, hsa-mir-324, hsa-mir-335, hsa-mir-345, hsa-mir-423, hsa-mir-483, hsa-mir-486-1, hsa-mir-146b, hsa-mir-202, hsa-mir-432, hsa-mir-494, hsa-mir-495, hsa-mir-193b, hsa-mir-497, hsa-mir-455, hsa-mir-545, hsa-mir-376a-2, hsa-mir-487b, hsa-mir-551a, hsa-mir-571, hsa-mir-574, hsa-mir-576, hsa-mir-606, hsa-mir-628, hsa-mir-629, hsa-mir-411, hsa-mir-671, hsa-mir-320b-1, hsa-mir-320c-1, hsa-mir-320b-2, hsa-mir-378d-2, hsa-mir-889, hsa-mir-876, hsa-mir-744, hsa-mir-885, hsa-mir-920, hsa-mir-937, hsa-mir-297, hsa-mir-1233-1, hsa-mir-1260a, hsa-mir-664a, hsa-mir-320c-2, hsa-mir-2861, hsa-mir-378b, hsa-mir-1260b, hsa-mir-378c, hsa-mir-1233-2, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, hsa-mir-664b, hsa-mir-378j, hsa-mir-486-2
A panel of five circulating miRNAs was observed to be upregulated in serum samples from infected patients (miR-202, miR-342-5p, miR-206, miR-487b, and miR-576-5p), showing high sensitivity and specificity for differentiation of pertussis patients and HC. [score:4]
[1 to 20 of 1 sentences]
79
[+] score: 4
In contrast, miRNAs hsa-mir-214 (p<0.0001), hsa-mir-342 (p<0.0004), hsa-mir-145 (p<0.009), hsa-mir-125b (p<0.078) and hsa-mir-181b (p<0.0047) were significantly upregulated in DCM compared to non-failing controls. [score:3]
NF); *p< 0.003 (miRNA-342, DCM vs. [score:1]
[1 to 20 of 2 sentences]
80
[+] score: 4
Analysis of the 3′ UTR of AR failed to find a binding site for miR-342 ([57] and data not shown), suggesting that suppression of AR by miR-342 may be not through the typical miRNA mediated mechanism. [score:3]
Tumors injected with miR-185 or 342 contained approximately 116±30-fold (miR-185, P < 0.05) or 278±59-fold (miR-342, P < 0.05) higher than the control tumors (Fig. 4B). [score:1]
[1 to 20 of 2 sentences]
81
[+] score: 4
Four other miRNAs (hsa-miR-342-5p, hsa-miR-194, hsa-miR-150, hsa-miR-132) were deregulated in the same and two miRNAs (hsa-miR-22*, hsa-miR-30e*) were deregulated in the opposite direction in whole blood and in one other cell subset. [score:4]
[1 to 20 of 1 sentences]
82
[+] score: 4
Compared to S/exo, the levels of miR-100, miR-17, miR-222, miR-342-3p and miR-451 were significantly up-regulated in A/exo and D/exo using qRT-PCR. [score:3]
Five miRNAs were selected for validation, all of which (miR-100, miR-17, miR-222, miR-342-3p and miR-451) were elevated in both A/exo and D/exo. [score:1]
[1 to 20 of 2 sentences]
83
[+] score: 4
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-mir-15a, hsa-mir-18a, hsa-mir-33a, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-107, mmu-mir-27b, mmu-mir-126a, mmu-mir-128-1, mmu-mir-140, mmu-mir-146a, mmu-mir-152, mmu-mir-155, mmu-mir-191, hsa-mir-10a, hsa-mir-211, hsa-mir-218-1, hsa-mir-218-2, mmu-mir-297a-1, mmu-mir-297a-2, hsa-mir-27b, hsa-mir-128-1, hsa-mir-140, hsa-mir-152, hsa-mir-191, hsa-mir-126, hsa-mir-146a, mmu-let-7a-1, mmu-let-7a-2, mmu-mir-15a, mmu-mir-18a, mmu-mir-103-1, mmu-mir-103-2, mmu-mir-342, hsa-mir-155, mmu-mir-107, mmu-mir-10a, mmu-mir-218-1, mmu-mir-218-2, mmu-mir-33, mmu-mir-211, hsa-mir-374a, gga-mir-33-1, gga-let-7a-3, gga-mir-155, gga-mir-18a, gga-mir-15a, gga-mir-218-1, gga-mir-103-2, gga-mir-107, gga-mir-128-1, gga-mir-140, gga-let-7a-1, gga-mir-146a, gga-mir-103-1, gga-mir-218-2, gga-mir-126, gga-let-7a-2, gga-mir-27b, mmu-mir-466a, mmu-mir-467a-1, hsa-mir-499a, hsa-mir-545, hsa-mir-593, hsa-mir-600, hsa-mir-33b, gga-mir-499, gga-mir-211, gga-mir-466, mmu-mir-675, mmu-mir-677, mmu-mir-467b, mmu-mir-297b, mmu-mir-499, mmu-mir-717, hsa-mir-675, mmu-mir-297a-3, mmu-mir-297a-4, mmu-mir-297c, mmu-mir-466b-1, mmu-mir-466b-2, mmu-mir-466b-3, mmu-mir-466c-1, mmu-mir-466e, mmu-mir-466f-1, mmu-mir-466f-2, mmu-mir-466f-3, mmu-mir-466g, mmu-mir-466h, mmu-mir-467c, mmu-mir-467d, mmu-mir-466d, hsa-mir-297, mmu-mir-467e, mmu-mir-466l, mmu-mir-466i, mmu-mir-466f-4, mmu-mir-466k, mmu-mir-467f, mmu-mir-466j, mmu-mir-467g, mmu-mir-467h, hsa-mir-664a, hsa-mir-1306, hsa-mir-1307, gga-mir-1306, hsa-mir-103b-1, hsa-mir-103b-2, gga-mir-10a, mmu-mir-1306, mmu-mir-3064, mmu-mir-466m, mmu-mir-466o, mmu-mir-467a-2, mmu-mir-467a-3, mmu-mir-466c-2, mmu-mir-467a-4, mmu-mir-466b-4, mmu-mir-467a-5, mmu-mir-466b-5, mmu-mir-467a-6, mmu-mir-466b-6, mmu-mir-467a-7, mmu-mir-466b-7, mmu-mir-467a-8, mmu-mir-467a-9, mmu-mir-467a-10, mmu-mir-466p, mmu-mir-466n, mmu-mir-466b-8, hsa-mir-466, hsa-mir-3173, hsa-mir-3618, hsa-mir-3064, hsa-mir-499b, mmu-mir-466q, hsa-mir-664b, gga-mir-3064, mmu-mir-126b, gga-mir-33-2, mmu-mir-3618, mmu-mir-466c-3, gga-mir-191
Previous studies revealed that five miRNA genes as well as their host genes (hsa-mir-10a/ HOXB4, hsa-mir-126/ EGFL7, hsa-mir-152/ COPZ2, hsa-mir-191/ DALRD3, and hsa-mir-342/ EVL) were found to be epigenetically downregulated, either by histone modification and/or CpG island hypermethylation in the promoter region in cancer cells [27], [86]– [89] (Table 2 ). [score:4]
[1 to 20 of 1 sentences]
84
[+] score: 4
Other miRNAs from this paper: hsa-mir-199a-1, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-214
EVL is the host gene of miR-342 which was down-regulated in SzS patients [42], and miR-342 is known to induce apoptosis. [score:4]
[1 to 20 of 1 sentences]
85
[+] score: 4
Wang SH Long non-coding RNA H19 regulates FOXM1 expression by competitively binding endogenous miR-342-3p in gallbladder cancerJ Exp Clin Cancer Res. [score:4]
[1 to 20 of 1 sentences]
86
[+] score: 4
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-mir-16-1, hsa-mir-17, hsa-mir-18a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-20a, hsa-mir-21, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-29a, hsa-mir-31, hsa-mir-99a, hsa-mir-100, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-106a, hsa-mir-16-2, hsa-mir-192, hsa-mir-199a-1, hsa-mir-208a, hsa-mir-30c-2, hsa-mir-147a, hsa-mir-10a, hsa-mir-34a, hsa-mir-181b-1, hsa-mir-199a-2, hsa-mir-203a, hsa-mir-204, hsa-mir-217, hsa-mir-219a-1, hsa-mir-221, hsa-mir-222, hsa-mir-223, hsa-mir-200b, hsa-mir-27b, hsa-mir-30b, hsa-mir-122, hsa-mir-125b-1, hsa-mir-132, hsa-mir-140, hsa-mir-142, hsa-mir-143, hsa-mir-145, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-146a, hsa-mir-150, hsa-mir-185, hsa-mir-193a, hsa-mir-195, hsa-mir-200c, hsa-mir-155, hsa-mir-181b-2, hsa-mir-30c-1, hsa-mir-219a-2, hsa-mir-296, hsa-mir-130b, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-302d, hsa-mir-374a, hsa-mir-375, hsa-mir-378a, hsa-mir-330, hsa-mir-328, hsa-mir-325, hsa-mir-424, hsa-mir-429, hsa-mir-450a-1, hsa-mir-486-1, hsa-mir-146b, hsa-mir-497, hsa-mir-520e, hsa-mir-520f, hsa-mir-520a, hsa-mir-520b, hsa-mir-520c, hsa-mir-520d, hsa-mir-520g, hsa-mir-520h, hsa-mir-450a-2, hsa-mir-503, hsa-mir-608, hsa-mir-625, hsa-mir-629, hsa-mir-663a, hsa-mir-1271, hsa-mir-769, hsa-mir-378d-2, hsa-mir-675, hsa-mir-147b, hsa-mir-374b, hsa-mir-663b, hsa-mir-378b, hsa-mir-378c, hsa-mir-374c, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, hsa-mir-4661, hsa-mir-219b, hsa-mir-203b, hsa-mir-378j, hsa-mir-486-2
In ApoE [−/−] mice, the inhibition of the proathero-miR-342-5p reduced atherosclerotic plaque development in the aorta of these animals [67]. [score:4]
[1 to 20 of 1 sentences]
87
[+] score: 3
24 *** hsa-mir-770-5p 19 *** 75.47 *** hsa-mir-93* 9.5 *** 92.1 - Inhibited differentiation & low cell count *** hsa-let-7b* 4.75 *** 28.64 *** hsa-mir-1224-3p 2.38 *** 51.46 *** hsa-mir-1228 2.38 ** 9.43 *** hsa-mir-1249 1.66 *** 53.17 *** hsa-mir-125a-5p 19 *** 69.8 *** hsa-mir-1260 7.12 *** 61.75 *** hsa-mir-1280 11.88 *** 68.95 *** hsa-mir-129-3p 9.5 *** 65.64 - hsa-mir-1296 9.5 *** 36.36 *** hsa-mir-133a/hsa-mir-133b 42.75 * 0.85 *** hsa-mir-150 4.75 *** 60.37 *** hsa-mir-197 4.75 *** 27.79 *** hsa-mir-204 2.85 *** 27.44 *** hsa-mir-328 0.1 ** 30.87 *** hsa-mir-342-3p 33.25 *** 58. [score:3]
[1 to 20 of 1 sentences]
88
[+] score: 3
Recent studies demonstrated that miR-138, miR-133a, miR-342, miR-491-5p, miR-541, miR-1207-5p, miR-1266 and miR-1182 control hTERT expression in leukemic T-cell lymphoblasts, gastric cancer, cervical cancer, thyroid carcinoma and head and neck squamous cell carcinoma [28– 31, 33]. [score:3]
[1 to 20 of 1 sentences]
89
[+] score: 3
Lerman et al. observed the expression of the following miRNAs in psoriatic lesion skin: hsa-miR-149, hsa-miR-150, hsa-miR-210, hsa-miR-220, hsa-miR-326, has-miR-324-5p, hsa-miR-342, hsa-miR-326, hsa-miR-328, hsa-miR-345, hsa-miR-346, and hsamiR-197 [20]. [score:3]
[1 to 20 of 1 sentences]
90
[+] score: 3
In addition, they showed expression trend that were the opposite of their related miRNAs, hsa-miR-330-3P, hsa-miR-342-3P, hsa-miR-501-3P, hsa-miR-331-3P, hsa-miR-340-3P, hsa-miR-3607-3P, hsa-miR-3614-3P and hsa-miR-374a-3P. [score:3]
[1 to 20 of 1 sentences]
91
[+] score: 3
In 2011, Roth et al profiled miRNA expression of peripheral blood mononuclear cells in 20 GBM patients and matched healthy volunteers with biochip containing 1158 human mature miRNAs, and found miR-128, miR-342-3p and a signature (consisting of 180 miRNAs) could be used to distinguish patients and healthy volunteers [16]. [score:3]
[1 to 20 of 1 sentences]
92
[+] score: 3
Alveolar macrophages possessed the highest number of highly expressed miRNAs than the other cell types and included miR-92, miR-223, miR-191, miR-30a-5p, miR-320, miR-342, miR-146b and miR-142-3p. [score:3]
[1 to 20 of 1 sentences]
93
[+] score: 3
Other miRNAs from this paper: mmu-mir-125a, hsa-mir-125a, mmu-mir-342, hsa-mir-1976, hsa-mir-4638
Based on context scores and context score percentile as well as the outcome from multiple program prediction analysis, certain miRNAs, such as hsa-miR-4638-5p, hsa-miR-342-5p, hsa-miR-1976, hsa-miR-125a-3p and others were predicted to efficiently target the SLC44A4 3’-UTR. [score:3]
[1 to 20 of 1 sentences]
94
[+] score: 3
Additionally, prior studies from various mo dels of retinal degeneration identified over 300 differentially expressed miRNAs 63– 90, a total of 16 common miRNAs were identified (miR-1187, miR-125b-5p, miR-331-3p, miR466d-3p, miR-467f, miR-542-3p, miR-574-5p, miR654-3p, miR669h-3p, miR-882, miR-342-3p, miR-466a-5p, miR-466d-5p, miR-706, miR-345-3p, miR532-5p). [score:3]
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95
[+] score: 3
The human panel of 157 miRNAs screened in the study included three other miRNAs located in this region, miR-134, miR-337, and miR-342, but their expression did not have any statistical significance associated with APML samples. [score:3]
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96
[+] score: 3
A role for HRMs in cytokine expression modulation has also been demonstrated for BMP2 (miR-106b, -20a, and miR-106a), Zinc finger and BTB domain containing 16 or ZBTB16 (miR-1271, miR-342), and Chemokine (C-X-C motif) ligand or CXCL3,6, and 8 (miR-106a/b, -20a, -493 and miR-425) via the HRMs indicated [49, 67, 68]. [score:3]
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97
[+] score: 3
Tao K. Yang J. Guo Z. Hu Y. Sheng H. Gao H. Yu H. Prognostic value of miR-221-3p, miR-342-3p and mir-491-5p expression in colon cancerAm. [score:3]
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98
[+] score: 3
Tao K. Yang J. Guo Z. Hu Y. Sheng H. Gao H. Yu H. Prognostic value of miR-221–3p, miR-342–3p and miR-491–5p expression in colon cancer Am. [score:3]
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99
[+] score: 3
We chose three specific miRNAs (miR-320a, miR-221, and miR-342) and further confirmed their enhanced expression in Beas2B epithelial MVs after hyperoxia (Fig. 5B). [score:3]
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100
[+] score: 2
None of those overlapped with the human urinary miRNAs in our study and one, miR-342-5p, was also found in kidney tissue to be associated to obstruction in the partial neonatal mouse mo del, however with an opposite regulation [39]. [score:2]
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