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50 publications mentioning mmu-mir-342

Open access articles that are associated with the species Mus musculus 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: 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: 172
In this work, we demonstrated that miR-342-5p and miR-608 directly targeted NAA10 mRNA and reduced the expression of NAA10, therefore inhibiting colon cancer tumorigenesis (Figure 7K). [score:8]
Our results showed that two miRNAs, miRNA-342-5p and miRNA-608, targeted the 3′-UTR of NAA10 mRNA for degradation, suppressed cell proliferation and migration, and promoted apoptosis by downregulating NAA10 levels. [score:8]
Here, we identified two new miRNAs (miR-342-5p and miR-608) targeting NAA10 mRNA for degradation and suppressing its expression. [score:7]
Although we have demonstrated that miR-342-5p and miR-608 suppresses tumorigenesis most likely by targeting NAA10, there may be other targets responsible for the effects of these two miRNAs, considering the low specificities of miRNAs. [score:7]
Thus, miRNA-342-5p and miR-608 suppress colon cancer tumorigenesis most likely by downregulating NAA10. [score:6]
MiR-342-5p and miR-608 suppress tumorigenesis by downregulating NAA10. [score:6]
Out of 12 candidates, only miR-342-5p and miR-608 significantly suppressed the luciferase signal (Figure 1B), indicating that these two miRNAs specifically target the NAA10 3′-UTR. [score:5]
Accordingly, we observed reduced expression of miR-342-5p and miR-608 in patient-derived colon cancer samples, which was inversely correlated with the expression of NAA10. [score:5]
Overexpression of miR-342-5p or miR-608 reduced NAA10 expression in vitro and in vivo. [score:5]
These results implied that miR-342-5p and miR-608 may both target NAA10 for degradation and thereby repress the expression of NAA10. [score:5]
Overexpression of NAA10 rescued the inhibition of colony formation and migration induced by miR-342-5p transfection in SW480 and SW620 cells (Figure 6B and 6C). [score:5]
MiR-342-5p and miR-608 directly targeted NAA10 for degradation. [score:4]
Sequence alignment revealed that the target sequence of miR-342-5p and miR-608 is conserved across species (Figure 2C). [score:3]
Our results suggest that NAA10 may serve as a potential target for colon cancer therapy, and miR-342-5p and miR-608 may have potential therapeutic applications in colon cancer patients. [score:3]
To further validate this conclusion, stable cell lines expressing miR-342-5p, miR-608, anti-342-5p, and anti-608 were generated and tested in a mouse xenograft mo del. [score:3]
MiR-342-5p and miR-608 regulate NAA10 by directly binding to its 3′UTR. [score:3]
MiR-342-5p and miR-608 suppressed cell proliferation, migration, and colony formation and promoted apoptosis in colon cancer cells. [score:3]
A., B. The mutant NAA10-3′-UTR luciferase vectors were constructed by mutating the conserved sequences targeted by miR-342-5p and miR-608 in the NAA10-3′-UTR luciferase vector as indicated. [score:3]
NAA10 restoration rescued miR-342-5p and miR-608 mediated cell proliferation, migration, and colony formation defects and promoted cell apoptosis suppressed by miR-342-5p or miR-608. [score:3]
We have previously shown that miR-342-5p and miR-608 suppress cell proliferation, colony formation cell-cycle progression and promote apoptosis. [score:3]
The human NAA10 3′UTR harboring three putative miR-342-5p and miR-608 target binding sequences was synthesized by GenPharm (Shanghai, China). [score:3]
MiR-342-5p and miR-608 repressed the tumorigenesis of colon cancer cells in vitroWe have previously verified miR-342-5p and miR-608 target NAA10. [score:3]
Lastly, we tested whether miR-342-5p or miR-608 overexpression affected cell survival. [score:3]
Overexpression of miR-342-5p or miR-608 significantly restrained the tumor growth by 4 weeks (Figure 5A and 5B), while anti-342-5p and anti-608 promoted tumor growth (Figure 5C and 5D). [score:3]
Anti-342-5p and anti-608 enhanced tumorigenesis of colon cancer cells in vitroWe have previously shown that miR-342-5p and miR-608 suppress cell proliferation, colony formation cell-cycle progression and promote apoptosis. [score:3]
Figure 2 A., B. The mutant NAA10-3′-UTR luciferase vectors were constructed by mutating the conserved sequences targeted by miR-342-5p and miR-608 in the NAA10-3′-UTR luciferase vector as indicated. [score:3]
We have previously verified miR-342-5p and miR-608 target NAA10. [score:3]
MiR-342-5p and miR-608 repressed tumorigenesis of colon cancer cells in vivoPreviously, we showed that miR-342-5p and miR-608 repressed cell proliferation, migration, colony formation, and cell-cycle progression, and promoted apoptosis in vitro, suggesting that miR-342-5p and miR-608 may serve as tumor suppressors. [score:3]
For orthotopic implantation, 1×10 [7] viable scramble, miR-342-5p, or miR-608 expressing cells were injected into CB-17 SCID mice colons in a volume of 0.1 ml. [score:3]
Collectively, these results indicate that NAA10 can partially rescue colon cancer tumorigenesis that is repressed by miR-342-5p or miR-608 overexpression in vitro. [score:3]
Overexpression of miR-342-5p or miR-608 reduced the proliferation of SW480 and SW620 cells (Figure 3A). [score:3]
Previously, we showed that miR-342-5p and miR-608 repressed cell proliferation, migration, colony formation, and cell-cycle progression, and promoted apoptosis in vitro, suggesting that miR-342-5p and miR-608 may serve as tumor suppressors. [score:3]
Figure 5MiR-342-5p and miR-608 suppressed colon cancer cell tumorigenesis in vivo A. Cells expressing scramble, miR-342-5p or miR-608 were orthotopically injected into the colons of SCID mice (7 per group), and the tumor volumes were assessed by bioluminescence (BLI) measurements at the indicated time points. [score:3]
MiR-342-5p and miR-608 suppressed colon cancer cell tumorigenesis in vivo. [score:3]
We have demonstrated that miR-342-5p and miR-608, the regulators of NAA10, also play important roles in such cellular processes; however, the underlying mechanism is not clear. [score:2]
These results further confirmed that NAA10 is involved in colon cancer tumorigenesis, and miR-342-5p and miR-608 participate in colon cancer tumorigenesis by regulating NAA10 (Figure 7K). [score:2]
NAA10 knockdown significantly decreased the proliferation of SW480 and SW620 cells, similar to the effects of miR-342-5p and miR-608 (Figure 7A-7C, 7F). [score:2]
MiR-342-5p and miR-608 can directly bind to the 3′-UTR of NAA10. [score:2]
These results demonstrated that miR-342-5p and miR-608 repressed NAA10 by directly binding to its 3′UTR. [score:2]
K. Mo del of the miR-342-3p and miR-608 regulate NAA10 in colon cancer cells. [score:2]
Lentiviral vectors for miR-342-5p, miR-608, anti-342-5p, anti-608 (40 ng, respectively) and their control vectors were purchased from Sigma. [score:1]
Cotransfection of NAA10 with miR-342-5p or miR-608 restored NAA10 levels (Figure 6A). [score:1]
These results suggested that anti-342-5p and anti-608 promoted tumorigenesis of colon cancer cells in vitro, and therefore further confirmed our finding that miR-342-5p and miR-608 repressed tumorigenesis of colon cancer cells in vitro. [score:1]
Consistent with our previous results, NAA10 protein levels declined when cells were transfected with miR-342-5p or miR-608 alone. [score:1]
A. Cells expressing scramble, miR-342-5p or miR-608 were orthotopically injected into the colons of SCID mice (7 per group), and the tumor volumes were assessed by bioluminescence (BLI) measurements at the indicated time points. [score:1]
MiR-342-5p, miR-608, anti-342-5p and anti-608 were purchased from Shanghai GenePharma (Shanghai, China). [score:1]
Meanwhile, neither miR-342-5p nor anti-342-5p had an effect on the mutant NAA10 luciferase activity (Figure 2D right). [score:1]
The relative levels of miR-342-5p and miR-608 were detected by stem-loop RT-PCR with following conditions: denaturing the DNA at 94°C for 4 min followed by 40 cycles for amplification: 94°C for 60 s, 58°C for 60 s, 72°C for 60 s. U6 snRNA was used as an endogenous control. [score:1]
Collectively, these results indicated that miR-342-5p and miR-608 repressed tumorigenesis of colon cancer cells in vitro. [score:1]
Cells transfected with either scramble miRNA, miR-342-5p or miR-608 were serum-starved overnight, and then subjected to flow cytometry analysis. [score:1]
NAA10 mRNA, miR-342-5p and miR-608 levels were determined by real-time PCR. [score:1]
In a mouse xenograft mo del, miR-342-5p and miR-608 efficiently repressed tumorigenesis of two colon cancer cell lines, SW480 and SW620. [score:1]
To further test the effects of miR-342-5p and miR-608 on tumorigenesis in vitro, we seeded a single cell in 6-well-plates and observed that cells transfected with miR-342-5p or miR-608 formed fewer colonies than cells transfected with a scramble miRNA control sequence (Figure 3B, 3C). [score:1]
In conclusion, our results suggested that miR-342-5p and miR-608 repressed tumor growth in vivo. [score:1]
In line with the previous results, miR-342-5p decreased the activity of the wild-type (WT) NAA10 luciferase reporter, which was rescued by anti-342-5p (Figure 2D left). [score:1]
MiR-342-5p and miR-608 repressed the tumorigenesis of colon cancer cells in vitro. [score:1]
Consistent with the NAA10 mRNA levels, NAA10 protein levels were reduced by miR-342-5p but increased by anti-342-5p in SW480 and SW620 cells (Figure 1E-1F). [score:1]
To verify this hypothesis, we co -transfected miR-342-5p and NAA10 into SW480 and SW620 cells. [score:1]
MiR-342-5p and miR-608 repressed tumorigenesis of colon cancer cells in vivo. [score:1]
The inverse correlations between NAA10 and the two miRNAs miR-342-5p and miR-608 were observed in the paired colon cancer samples and adjacent normal mucosa tissues (Figure 7H, 7I). [score:1]
To further confirm these results, miR-342-5p and miR-608 antisense sequences were synthesized (referred to as anti-342-5p and anti-608). [score:1]
NAA10 restoration significantly reduced apoptosis induced by serum-starvation in cells transfected with miR-342-5p (Figure 6D). [score:1]
The percentage of cells in S-phase and G2/M-phase declined when cells were transfected with miR-342-5p or miR-608, respectively, in both SW480 (Figure 3D) and SW620 cells (Figure 3E). [score:1]
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[+] score: 127
Likewise, miR-342 inhibits Myc activity via regulation of E2F1 (19) and inhibits apoptosis in breast cancer cell lines via regulation of Apollon/BRUCE (20) or the human epidermal growth factor receptor 2 (HER2) pathway and inhibited the proliferation of HER2 -positive cell lines (21). [score:9]
The expression changes observed in miR-342 in multiple cancers may still serve as diagnostic targets with clinical benefits; indeed, expression of miR-342 has been observed to correlate with postoperative survival in pancreatic cancer (29) and response to tamoxifen treatment in breast cancer (30). [score:7]
Finally, miR-342 expression in the surrounding stroma may provide a tumor-suppressing function via enhancing the inhibitory effect of TGFβ on angiogenesis (27). [score:7]
The selection cassette was removed from the targeted allele by transient transfection of a Cre recombinase expression plasmid and the ES cells were used to generate miR-342 knockout mice in the C57Bl/6N genetic background. [score:6]
The breadth of cancers observed to show expression changes in miR-342 suggests a common oncogenic function for these changes, mediated by altered regulation of the target mRNA. [score:6]
miR-342-3p suppresses proliferation, migration and invasion by targeting FOXM1 in human cervical cancer. [score:5]
Together, the expression and functional data indicate miR-342 as a tumor-suppressor-miR. [score:5]
Based on expression changes in cancer, miR-342 has been proposed as both an onco-miR and, more commonly, a tumor-suppressor-miR. [score:5]
For example, miR-342 inhibits proliferation and invasiveness of non-small cell lung cancer cell lines after transfer into nude mice via regulation of RAP2B (18). [score:4]
Ela1-Tag mice (28, 35), with transgenic expression of the SV40 large T Antigen under the Elastase-1 promoter, were purchased from Jackson on the C57BL/6 background and backcrossed to miR-342 knockout mice. [score:4]
In hepatocellular carcinoma cell lines, miR-342 inhibits proliferation by regulating the NF-κB pathway (26). [score:4]
The regulation of FOXM1 by miR-342 has also been proposed to be important for cervical cancer, with a function in inhibiting growth and metastasis in HeLa transplant mo dels (25). [score:4]
The miR-342 knockout allele was generated as a 197bp targeted deletion generated in C57Bl/6N JMA. [score:4]
miR-342 has been demonstrated to inhibit the tumorigenic capacity in transplanted colon cancer cell lines, a role attributed to regulation of NAA10 (22), DNA methyltransferase 1 (23), or FOXM1 and FOXQ1 (24). [score:4]
During functional testing, the roles identified for miR-342 have been largely tumor-suppressing in nature, with repression of key oncogenic proteins. [score:3]
Figure 1Pancreatic acinar carcinoma development in miR-342 knockout mice. [score:3]
In addition, even the extent to which murine miR physiology mimics that of the human is unclear, with mRNA exhibiting lower levels of miR recognition conservation than protein sequence conservation (32) [although many of the predicted oncogenic targets of miR-342 are conserved from mouse to human (33)]. [score:3]
While these results do not encourage the exploration of miR-342 as a clinical target in pancreatic cancer, neither do they disqualify it. [score:3]
Through longitudinal magnetic resonance imaging (MRI) assessment, we found no evidence for a tumor-suppressor role for miR-342 in the Ela1-TAg transgenic mo del. [score:3]
It should, however, be noted that miR-342 expression is coordinated with the host gene, EVL (17), and thus even if the observed correlation is functional it may not indicate an oncogenic role specific to miR-342. [score:3]
It therefore remains distinctly possible that further preclinical exploration will support miR-342 as a valid target for clinical intervention in a subset of pancreatic cancer patients with the appropriate molecular distortions (2). [score:3]
The resulting miR-342 [0/0] TAg [+] mice, and the parental TAg [+] strain, develop spontaneous pancreatic acinar carcinoma (Figure 1A), in which miR-342 expression was specifically lost in the KO (Figure 1B). [score:3]
The function of miR-342 in the development, growth, and pathogenicity of pancreatic cancer was tested by newly generating miR-342 [0/0] mice and intercrossing with the Ela1-TAg transgenic mouse (28). [score:2]
Figure 3Normal tumor onset in miR-342 knockout mice. [score:2]
Figure 4Tumor growth rates are unaffected in miR-342 knockout mice using a pancreatic cancer mo del. [score:2]
This resulted in normal cumulative incidence of pancreatic cancer in both female (Figure 3B) and male (Figure 3C) mice, indicating no significant effect of miR-342 in pancreatic cancer development in this mo del. [score:2]
Figure 2Longitudinal monitoring of tumor growth in miR-342 knockout mice. [score:2]
Expression of mature miR-342 was determined using TaqMan™ MicroRNA Assays (hsa-miR-342-3p; Applied Biosystem). [score:2]
Figure 5Tumor -induced mortality is unaffected in miR-342 knockout mice. [score:2]
Together, these results indicate that there is no major function for miR-342 in the development, growth, or pathogenicity of pancreatic cancer in the Ela1-TAg mo del. [score:2]
Both miR-342 and EVL are poorly characterized; however, miR-342 is proposed to have important oncogenic functions, with differential expression in pancreatic cancer (5) as well as acute myeloid leukemia (6, 7), breast cancer (triple -negative (8), inflammatory (9), or recurrent (10) subtypes), cervical cancer (11), colorectal cancer (12, 13), lung adenocarcinoma (14), lymphoma (15), and metastatic melanoma (16). [score:1]
Pancreatic tumors were dissected from TAg [+], miR-342 [+/0] TAg [+], and miR-342 [0/0] TAg [+] mice at 21 weeks of age. [score:1]
In miR-342-sufficient mice, tumors increased in size ±500% every 14 days, with no significant change in the growth rate observed with miR-342-deficiency, in either males or females (Figure 4G). [score:1]
TAg [+], miR-342 [+/0] TAg [+], and miR-342 [0/0] TAg [+] mice were monitored longitudinally by magnetic resonance imaging for tumor presence. [score:1]
No significant difference in age of first tumor detection was induced by heterozygous or homozygous loss of miR-342 (Figure 3A). [score:1]
No excess mortality was observed within this time period in miR-342 [+/0] TAg [+] or miR-342 [0/0] TAg [+] mice (Figure 5), although the limited time frame of observation does not exclude effects on survival after 21 weeks of age. [score:1]
Furthermore, our results, while negative, do not exclude a functional role for miR-342 in pancreatic cancer—the TAg mo del is just one of many increasingly sophisticated pancreatic cancer mo dels, which more closely mo del the most common genetic insults observed in patient specimens (31). [score:1]
miR-342 is an intronic miR located within the host gene EVL. [score:1]
Total tumor volumes were square root transformed, with plots showing individual growth in total tumor burden from point of first detection in (A) TAg [+] female mice (n = 10), (B) miR-342 [+/0] TAg [+] female mice (n = 8), (C) miR-342 [0/0] TAg [+] female mice (n = 6), (D) TAg [+] male mice (n = 13), (E) miR-342 [+/0] TAg [+] male mice (n = 6), and (F) miR-342 [0/0] TAg [+] male mice (n = 4). [score:1]
TAg [+], miR-342 [+/0] TAg [+], and miR-342 [0/0] TAg [+] mice were monitored longitudinally by magnetic resonance imaging for tumor load and size, from 7 weeks of age until 21 weeks of age. [score:1]
TAg [+], miR-342 [+/0] TAg [+], and miR-342 [0/0] TAg [+] mice were monitored longitudinally by magnetic resonance imaging (MRI) for tumor load and size, from 7 weeks of age until 21 weeks of age. [score:1]
TAg [+], miR-342 [+/0] TAg [+], and miR-342 [0/0] TAg [+] mice were followed until 21 weeks of age. [score:1]
Here, we sought to determine the in vivo functional role of miR-342 in a spontaneous murine mo del of pancreatic acinar carcinoma. [score:1]
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[+] 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: 66
Wnt10b, a putative target gene of miR-342-3p, and Wnt11 targeted by miR-188-5p were upregulated in the fibrotic liver, although the expression of miR-342-3p and miR-188-5p were elevated. [score:10]
To validate the data of the miRNA array, we conducted real-time quantitative reverse transcriptional polymerase chain reaction (qRT-PCR) for the expression of six upregulated miRNAs (mmu-miR-574-5p, mmu-miR-466i, mmu-miR-342-3p, mmu-let-7i, mmu-miR-34a and mmu-miR-188-5p) and five downregulated miRNAs (mmu-miR-378a-3p, mmu-miR-202, mmu-miR-378b, mmu-miR-378d and mmu-miR-212-3p) in liver tissues from the CCl [4] group (n = 5) and the control group (n = 4). [score:9]
On the other hand, the expression of Ihh, Wnt10b and Wnt11 was elevated with the increase of their regulatory miRNAs, miR-34a, miR-342-3p and miR-188-5p, respectively, and the level of Wnt6 was reduced with the decrease of its regulator miRNA, miR-378, in the CCl [4] group, implying that other regulatory factors might be additionally involved in the expression of these genes. [score:8]
Interestingly, five miRNAs, including three upregulated miRNAs (let-7i, miR-188-5p and miR-342-3p) and two downregulated miRNAs (miR-202-3p and miR-378), were related to 5830404H04Rik, a C2 calcium -dependent domain containing 2 (C2cd2). [score:7]
Of the putative target genes, 231 target genes were predicted to be modulated by miR-342-3p, which was reported to control lipogenesis and cholesterogenesis by targeting SREBP-1, a key transcription factor for lipogenesis-related genes, such as fatty acid synthase (FASN) and 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR). [score:7]
Hhip, a well-established Hh inhibitor [22, 23], was analyzed to be targeted by miR-342-3p, and its expression was reduced with the increase of miR-342-3p during liver fibrosis (Table 1, Figure 2 and Figure 6). [score:7]
Among these 12 miRNAs, seven miRNAs, including 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, whereas five miRNAs, including mmu-miR-378a-3p, mmu-miR-202-3p, mmu-miR-378b, mmu-miR-378d and mmu-miR-212-3p, were downregulated in CCl [4] compared to the control group (Table 1). [score:6]
As the expression of Hhip was lowered, its putative regulator miR-342-3p and the RNA level of Ihh and Gli3 were significantly elevated in the CCl [4] group compared to the control group (p < 0.05). [score:3]
In addition, the RNA level of Gas1, Prkacb, Stk36 and Wnt9a significantly decreased as the expression of their regulatory miRNAs, miR-188-5p for Gas1, miR-34a for Prkacb, let-7i for Stk36 and let-7i and miR-342-3p for Wnt9a, increased in the CCl [4] group compared to the control group. [score:3]
These findings imply that the activation of Ihh -mediated Hh signaling may be promoted by miR-342-3p -mediated inhibition of Hhip during liver fibrosis. [score:3]
Prkaa2, one of the core target genes (Figure 3B) related to miR-378, miR-342-3p, miR-188-5p and let-7i, seems to be involved in the FoxO signaling pathway, mTOR signaling pathway, PI3K-Akt signaling pathway, AMPK signaling pathway, insulin signaling pathway and the adipocytokine signaling pathway. [score:3]
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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: 38
As shown, the expression levels of miR-342 and miR-455 in SV were significantly downregulated, while miR-29a and miR-203 were upregulated when compared to those of the P21 mice. [score:8]
Two upregulated (miR-29a and miR-203) and two downregulated (miR-342 and miR-455) miRNAs shown in the microarray analyses were selected for q-PCR analysis. [score:7]
Among the list, members of the miR-29 family, miR-203, miR-762, and miR-1224, showed upregulation, whereas members of the miR-107 family, miR-127 and miR-130a/b, miR-342-3p, miR-351, miR-379, miR-455, and miR-467a, were downregulated in both strains. [score:7]
Notably, our data revealed that expression of Tnfsf10 (upregulated by ∼2-fold) is likely influenced by several miRNAs including miR-107, miR-145, miR-342-3p, miR-491, miR-494, miR-182, and miR-467a. [score:6]
Similarly, miR-342 was also downregulated and has been shown to regulate melanogenesis [70]. [score:5]
The four downregulated miRNAs are miR-107, miR-145, miR-342, and miR-455. [score:4]
These miRNAs include miR-107, miR-127, miR-130a/b, miR-145, miR-342, miR-351, miR-379, miR-455, and miR-467. [score:1]
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While opposite trends in expression patterns exists between these two miRNAs, remembering that miRNAs bind to a target gene to elicit action, the greater relative fold change of miR-342-5p may be producing diminished protein expression of Tceanc, as well as other genes, in the high-active animals. [score:7]
In the nucleus accumbens, miR-342-5p was found to be upregulated (∼115 fold) and miR-466 was downregulated (∼4 fold) in the high-active mice. [score:7]
Furthermore, miR-342-5p and miR-466 in the nucleus accumbens, and miR-466 in soleus were validated by qRT-PCR to be differentially expressed between the high- and low-active mice. [score:3]
Specifically, Keller, et al. (Keller et al. 2011) notes that SOX9 was involved in muscle adaption to aerobic training; SOX9 was a target for both miR-342-3p, and miR-466d-3p in this study as well. [score:3]
Of the 13 differentially expressed miRNAs, miR-342-5p (P < 0.0001; Fig. 1A) and miR-466d-3p (P = 0.0004; Fig. 1B) were chosen for validation by qRT-PCR. [score:3]
In the nucleus accumbens, miR-342-5p and miR-466 were validated as differentially expressed between strains by qRT-PCR, as was miR-466 in the soleus. [score:3]
Figure 1Relative expression determined by qRT-PCR of (A) miR-342-5p (P < 0.0001) and (B) miR-466 (P < 0.0004) in nucleus accumbens and (C) miR-466 (P < 0.0001) and (D) miR-1960 (P = 0.06) in the soleus between high- (C57L/J) and low- (C3H/HeJ) active mice. [score:3]
CamKII is a putative target gene for miR-669f-3p, miR-342-3p, and miR-466d-3p in the nucleus accumbens. [score:3]
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The microRNA expression levels of miR-18a-5p and miR-466f were down-regulated in the aged thymus, while the microRNA expression levels of miR342-3p, miR-6931-5p, miR-125a-5p and miR-320-5p were up-regulated in the aged thymus. [score:11]
Results are shown in Figure 2. In those 12 miRNAs, there were 6 miRNAs with statistically different expression, among which two (miR-18a-5p, miR-466f) were down-regulated (< -2.0 folds) in aged TECs which were consistent the result with ones in the microarray (Fig. 2 top panels), and four (miR-342-3p, miR-6931-5p, miR-125a-5p, miR320-5p) were up-regulated (> 2.0-fold), confirmed the trend in the microarray data (Fig. 2 middle and bottom panels). [score:9]
We did not find targeting sites of miR-6931-5p and miR-342-3p in FoxN1 3′UTR, while we found that miR-320-3p and miR-125a-5p have 3 and 5 targeting sites in FoxN1 3′UTR, respectively (Fig. 3). [score:5]
The microRNA expression levels of miR-18a-5p, miR-466f, miR342-3p, miR-6931-5p, miR-125a-5p and miR-320-5p were consistent with the miRNA microarray results. [score:3]
Figure 2. The microRNA expression levels of miR-18a-5p, miR-466f, miR342-3p, miR-6931-5p, miR-125a-5p and miR-320-5p were consistent with the miRNA microarray results. [score:3]
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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: 21
These include on the one hand the up-regulated miRNAs: mmu-miR-342-3p, mmu-miR-142-3p, mmu-miR-142-5p, mmu-miR-21, mmu-miR-335-5p, mmu-miR-146a, mmu-miR-146b, mmu-miR-674 and mmu-miR-379; and on the other hand the down-regulated ones after HFD -induced obesity: mmu-miR-122, mmu-miR-133p, mmu-miR-1, mmu-miR-30a, mmu-miR-192 and mmu-miR-203. [score:7]
Mmu-miR-342-3p and mmu-miR-379 were both found to be up-regulated after HFD -induced obesity in the present study. [score:4]
The following miRNAs were found to be up-regulated in WAT after HFD feeding: mmu-miR-342-3p, mmu-miR-222, mmu-miR-221, mmu-miR-142-3p, mmu-miR-142-5p, mmu-miR-21, mmu-miR-335-5p, mmu-miR-146a, mmu-miR-146b, mmu-miR-647* and mmu-miR-379. [score:4]
The following 22 murine microRNAs were selected for qPCR validation of their expression: mmu-miR-1, mmu-miR-21, mmu-miR-30a*, mmu-miR-30e*, mmu-miR-122, mmu-miR-130a, mmu-miR-133b, mmu-miR-141, mmu-miR-142-3p, mmu-miR-142-5p, mmu-miR-146a, mmu-miR-146b, mmu-miR-192, mmu-miR-193a-3p, mmu-miR-200b, mmu-miR-200c, mmu-miR-203, mmu-miR-204, mmu-miR-222, mmu-miR-342-3p, mmu-miR-378 and mmu-miR-379. [score:3]
A possible link between mmu-miR-342-3p and obesity is the glucagon that is a potential target of this miRNA and is implicated in obesogenesis [40]. [score:3]
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[+] score: 16
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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14
[+] score: 16
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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15
[+] score: 15
Similarly, 342 genes potentially downregulated (targets of mmu-miR-128 and mmu-miR-342-5p) and 200 potentially upregulated genes (targets of mmu-miR-465c-5p, mmu-miR-466d-3p, mmu-miR-466d-5p, mmu-miR-665, mmu-miR-683) in the colon were identified (Table S4). [score:11]
qRT-PCR was performed using SYBR Green qPCR Master Mix (Fermentas) on a Mastercycler Realplex [4] (Eppendorf) using the following primers:For mature miRNA expression: the universal primer provided in the NCode [TM] miRNA first-strand cDNA synthesis kit was used together with one of the following forward primer: mmu-miR-665: 5′-ACCAGG AGG CTG AGG TCC CT-3′mmu-miR-128: 5′-TCACAGTGAACCGGTCTCTTT-3′ mmu-mir-200c*: 5′-CGTCTTACCCAGCAGTGTTTGG-3′ mmu-miR-342-5p: 5′-AGGGGTGCTATCTGTGATTGAG-3′ mmu-miR-466d-3p: 5′-TATACATACACGCACACATAG-3′ mmu-miR-466d-5p: 5′-TGTGTGTGCGTACATGTACATG-3′ mmu-miR-465c-5p: 5′-TATTTAGAATGGCGCTGATCTG-3′ mmu-miR-683: 5′-CCTGCTGTAAGCTGTGTCCTC-3′ mmu-miR-665: 5′-ACCAGGAGGCTGAGGTCCCT-3′ mmu-miR-298: 5′-GGCAGAGGAGGGCTGTTCTTCCC-3′ For Abcc3 expression:Forward 5′-CTT CTT TTC CCG CTT GTC TTT-3′;Reverse 5′- CCT CCT CAG ACA GAG ACC AGA-3′. [score:2]
qRT-PCR was performed using SYBR Green qPCR Master Mix (Fermentas) on a Mastercycler Realplex [4] (Eppendorf) using the following primers: For mature miRNA expression: the universal primer provided in the NCode [TM] miRNA first-strand cDNA synthesis kit was used together with one of the following forward primer: mmu-miR-665: 5′-ACCAGG AGG CTG AGG TCC CT-3′ mmu-miR-128: 5′-TCACAGTGAACCGGTCTCTTT-3′ mmu-mir-200c*: 5′-CGTCTTACCCAGCAGTGTTTGG-3′ mmu-miR-342-5p: 5′-AGGGGTGCTATCTGTGATTGAG-3′ mmu-miR-466d-3p: 5′-TATACATACACGCACACATAG-3′ mmu-miR-466d-5p: 5′-TGTGTGTGCGTACATGTACATG-3′ mmu-miR-465c-5p: 5′-TATTTAGAATGGCGCTGATCTG-3′ mmu-miR-683: 5′-CCTGCTGTAAGCTGTGTCCTC-3′ mmu-miR-665: 5′-ACCAGGAGGCTGAGGTCCCT-3′ mmu-miR-298: 5′-GGCAGAGGAGGGCTGTTCTTCCC-3′ For Abcc3 expression: Forward 5′-CTT CTT TTC CCG CTT GTC TTT-3′; Reverse 5′- CCT CCT CAG ACA GAG ACC AGA-3′. [score:2]
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[+] score: 13
Following chronic CS exposure, 12 miRNAs (miR-146a, miR-148a, miR-152, miR-21, miR-26a, miR-30a-5p, miR-30c, miR-31, miR-31*, miR-342-3p, miR-376b* and miR-449) were differentially expressed in both lung tissue and BAL supernatant of which 10 showed concordant up- or down-regulation. [score:6]
Although detected in both human sputum and murine BAL supernatant, some miRNAs were expressed in the opposite direction such as miR-146a, miR-342-3p and miR-150 [8]. [score:4]
By focusing on the overlap between subacute and chronic CS exposure within the same compartment, or the overlap between miRNAs with altered expression levels in BAL and lung, we narrowed the pool of interesting miRNAs down to 18: let-7b, let-7c, miR-135b, miR-138, miR-146a, miR-148a, miR-152, miR-155, miR-21, miR-26a, miR-30a-5p, miR-30c, miR-31, miR-31*, miR-322*, miR-342-3p, miR-376b* and miR-449. [score:3]
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[+] score: 12
Aberrant Expression of miRNAs in Lin [−]c-Kit [+] Cells of Mice Exposed to BenzeneWe detected the expression of 8 miRNAs (mmu-miR-129b-5p, mmu-miR-451a, mmu-miR-34a-5p, mmu-miR-144-5p, mmu-miR-342-3p, mmu-miR-100-5p, mmu-miR-181a-5p, and mmu-miR-196b-5p) in Lin [−]c-Kit [+] cells through qRT-PCR. [score:5]
We detected the expression of 8 miRNAs (mmu-miR-129b-5p, mmu-miR-451a, mmu-miR-34a-5p, mmu-miR-144-5p, mmu-miR-342-3p, mmu-miR-100-5p, mmu-miR-181a-5p, and mmu-miR-196b-5p) in Lin [−]c-Kit [+] cells through qRT-PCR. [score:3]
In agreement with the sequencing data, the expression levels of mmu-miR-129b-5p, mmu-miR-451a, mmu-miR-34a-5p and mmu-miR-144-5p increased in the benzene exposure group, whereas the levels of mmu-miR-342-3p, mmu-miR-100-5p, mmu-miR-181a-5p, and mmu-miR-196b-5p decreased in the benzene exposure group (Figure 3). [score:3]
Of these miRNAs, five miRNAs, including mmu-miR-34a-5p, mmu-miR-342-3p, mmu-miR-100-5p, mmu-miR-181a-5p and mmu-miR-196b-5p, significantly changed in mice exposed to benzene. [score:1]
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[+] score: 10
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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[+] 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]
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[+] score: 9
However, we determined that miR-342-3p is expressed at low levels in the hippocampal CA1 neurons while a greater expression of this miRNA was observed in cerebellar granule neurons (data not shown). [score:5]
Of note, we were unable to detect miR-494-3p or miR-342-3p to be deregulated in our samples at clinical disease, both of which were detected in scrapie infected mice [49] and in BSE-infected macaques, a mo del for CJD [140]. [score:4]
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[+] 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]
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[+] score: 9
Treatment days miRNAExpression change [#] Predicted mRNA target(s)Expression change [#]GD 8/11 [†] miR-1192 ↑ Atf1, Gng4, Map3k1, Rpe, Setd2, Stxbp6, Zc3h6 ↓ miR-532-5p ↑ Atf1, Itpripl2, Stxbp6 ↓GD 14/16 [*] miR-10b ↓ Aak1 ↑ miR-184 ↓ Myl9 ↑ miR-302c ↑ Ccdc6, Mfap3, Ptpro, Rnd3, Rpl36a/r, Sema3c, Stoml3, Supt3h ↓ miR-342-5p ↓ Aak1, Cables2, Rhog ↑ miR-343 ↑ Asic4, Dcn, Gpr116, Ptpro, Stoml3 ↓ miR-449b ↓ Ina ↑PD 4/7 [†] miR-26b ↑ Adam9, Chsy1, Cnr1, Exoc8, Hs6st1, Lingo1, Map3k7, Mras, Pfkfb3, Ppm1b, Rhou, Sema6d, Shank2, Tab3, Tdrd7, Ube2j1 ↓ miR-34b-5p ↓ Kitl ↑ miR-184 ↑ Ncor2, Prkcb ↓ miR-721 ↑ Akap11, B4galt, Cnr1, Efnb2, Fam20b, Ino80, Irf1, Lrrk2, Ncoa3, Pfkfb3, Ppargc1a, Rbm9, Shank2, Spen, Sphk2, Tsc1, Wdfy3 ↓ miR-1970 ↓ Arhgap6 ↑ # Significance for expression change was 1.2-fold, p < 0.05. [score:9]
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[+] 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]
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[+] score: 7
Most notable, among the up-regulated miRNAs were miR-205, miR-342 and miR-21, while miR-29c, miR-192, miR-30b and miR-200a were significantly down-regulated. [score:7]
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[+] score: 7
We confirmed that six of the eight selected down-regulated hsa-miRNAs (miR-145, miR-497, miR-150, miR-342-5p, miR-34b* and miR-100) were significantly down-regulated in NPC tissues, whereas miR-195 and miR-143 exhibited no significant difference between the two groups of subjects (Fig. 1D). [score:7]
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[+] 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]
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[+] score: 6
With the exception of miR-150 and miR-342-3p, the majority of the miRs were down regulated in the DN subset. [score:2]
MiR-125b-5p, miR-150, miR-205, and miR-342-3p were consistently up regulated in the thymic tissue from the LPS injected mice (Figure 2B). [score:2]
MiR-709, miR-1224, and miR-342-3p/5p are increased several-fold in the DP subset, while miR-150 and miR-342-3p are increased in all the thymocyte subsets. [score:1]
The individual miRs (miR-15a, miR-17, miR-20a, miR-20b, miR-26b, miR-106a, miR-125-5p, miR-342-3p) were detected by Northern blotting. [score:1]
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[+] score: 6
In our PAH mice mo del, miR-328, miR-210, miR-342, and miR-125 were also downregulated in addition to miR-29b. [score:4]
The microarray profile revealed that several miRNAs, including miR-328a, miR-99b, miR-210, miR-342, miR-29b, miR-224, and miR-339, were regulated at different time points. [score:2]
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[+] 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]
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[+] score: 5
Interestingly, we noted significant up-regulation of miR-342-3p which is also one of three de-regulated miRNAs independently identified in the brains of BSE-infected macaques (Dirk Motzkus, German Primate Center, personal communication). [score:5]
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[+] 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]
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[+] score: 5
miR-155 is required for α-syn -induced inducible nitric oxide synthase (iNOS) expression in microglia in mo dels of PD [14], while three of these miRNAs (miR-125b-5p, miR-342-3p, and miR-99a) were specifically expressed in microglia [15]. [score:5]
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[+] score: 5
Other miRNAs from this paper: mmu-mir-30a, mmu-mir-101a, mmu-mir-125a, mmu-mir-125b-2, mmu-mir-132, mmu-mir-134, mmu-mir-135a-1, mmu-mir-138-2, mmu-mir-142a, mmu-mir-150, mmu-mir-154, mmu-mir-182, mmu-mir-183, mmu-mir-24-1, mmu-mir-194-1, mmu-mir-200b, mmu-mir-122, mmu-mir-296, mmu-mir-21a, mmu-mir-27a, mmu-mir-92a-2, mmu-mir-96, rno-mir-322-1, mmu-mir-322, rno-mir-330, mmu-mir-330, rno-mir-339, mmu-mir-339, rno-mir-342, rno-mir-135b, mmu-mir-135b, mmu-mir-19a, mmu-mir-100, mmu-mir-139, mmu-mir-212, mmu-mir-181a-1, mmu-mir-214, mmu-mir-224, mmu-mir-135a-2, mmu-mir-92a-1, mmu-mir-138-1, mmu-mir-181b-1, mmu-mir-125b-1, mmu-mir-194-2, mmu-mir-377, mmu-mir-383, mmu-mir-181b-2, rno-mir-19a, rno-mir-21, rno-mir-24-1, rno-mir-27a, rno-mir-30a, rno-mir-92a-1, rno-mir-92a-2, rno-mir-96, rno-mir-100, rno-mir-101a, rno-mir-122, rno-mir-125a, rno-mir-125b-1, rno-mir-125b-2, rno-mir-132, rno-mir-134, rno-mir-135a, rno-mir-138-2, rno-mir-138-1, rno-mir-139, rno-mir-142, rno-mir-150, rno-mir-154, rno-mir-181b-1, rno-mir-181b-2, rno-mir-183, rno-mir-194-1, rno-mir-194-2, rno-mir-200b, rno-mir-212, rno-mir-181a-1, rno-mir-214, rno-mir-296, mmu-mir-376b, mmu-mir-370, mmu-mir-433, rno-mir-433, mmu-mir-466a, rno-mir-383, rno-mir-224, mmu-mir-483, rno-mir-483, rno-mir-370, rno-mir-377, mmu-mir-542, rno-mir-542-1, mmu-mir-494, mmu-mir-20b, mmu-mir-503, rno-mir-494, rno-mir-376b, rno-mir-20b, rno-mir-503-1, mmu-mir-1224, mmu-mir-551b, mmu-mir-672, mmu-mir-455, mmu-mir-490, 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-504, mmu-mir-466d, mmu-mir-872, mmu-mir-877, rno-mir-466b-1, rno-mir-466b-2, rno-mir-466c, rno-mir-872, rno-mir-877, rno-mir-182, rno-mir-455, rno-mir-672, mmu-mir-466l, mmu-mir-466i, mmu-mir-466f-4, mmu-mir-466k, mmu-mir-466j, rno-mir-551b, rno-mir-490, rno-mir-1224, rno-mir-504, mmu-mir-466m, mmu-mir-466o, mmu-mir-466c-2, mmu-mir-466b-4, mmu-mir-466b-5, mmu-mir-466b-6, mmu-mir-466b-7, mmu-mir-466p, mmu-mir-466n, mmu-mir-466b-8, rno-mir-466d, mmu-mir-466q, mmu-mir-21b, mmu-mir-21c, mmu-mir-142b, mmu-mir-466c-3, rno-mir-322-2, rno-mir-503-2, rno-mir-466b-3, rno-mir-466b-4, rno-mir-542-2, rno-mir-542-3
NR5A1 was predicted to be the target gene of miR-342, while LDL-R was predicted to be the target gene of miR-182 and miR-466b. [score:5]
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[+] score: 4
As part of an inflammatory response the expression of miR-155 can also be increased indirectly through miR-342-5p [29], which was also induced in infected RAW264.7 cells and may have therefore contributed to the increase in miR-155 following MNV infection. [score:4]
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[+] score: 4
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 Antiviral Res. [score:4]
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[+] 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, 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, hsa-mir-342, 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]
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[+] score: 4
HF diet -associated miRNA up- (miR-22, miR-342-3p, miR-142-3p and others) and down-regulations (miR-200b, miR-200c, miR-204 and others) were observed in the adipose tissues of C57BL/6J mice [76]. [score:4]
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We found the miRNAs miR-146a-5p, miR-342-3p, miR-182-5p and miR-125a-3p to be subject to significant (p<0.05) differential expression between WT and MyD88 [-/-] BMMs (Fig 1C). [score:3]
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In contrast among the miRNAs which were altered in one group only, only miR-183-5p and miR-342-3p showed consistent trend of altered expression by comparing qRT-PCR result with sequencing (Figure S1A). [score:3]
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Among the miRNAs in the plasma, many have been shown to have differential expression in cells or tissue after ionizing radiation, such as miR-142-5p [27], miR-339, hsa-miR-342, hsa-miR146a, hsa-miR-29c, hsa-miR155, hsa-miR-197, hsa-miR-34b [28], and miR-29c [29]. [score:3]
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Other miRNAs from this paper: mmu-mir-125a, hsa-mir-125a, hsa-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]
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Similarly, we found an increased expression of let-7i-5p, miR-29a-3p, miR-29c-3p, miR-30a-5p, miR-98-5p, miR-138-5p, miR-139-5p, miR-140-5p, miR-146b-5p, miR-148b-3p, miR-181a-1-3p, miR-181a-5p, miR-194-5p, and miR-342-3p, all of which have been reported to be altered in different AD tissues (Cogswell et al., 2008; Hebert et al., 2008; Maes et al., 2009; Wang et al., 2011, 2012; Lau et al., 2013). [score:3]
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Similar Treg therapies are being used to treat diabetes (7) and could be used to restore normal expression of miR-342, miR-191, and miR-510 in Treg from diabetes patients (68). [score:3]
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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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[+] 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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miR-296-3p, miR-125a-5p, miR-342 and miR-486 have all been shown to be regulated by retinoic acid (Figure 2; Additional file 4). [score:2]
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Moreover, levels of miR-342-3p, miR-125b-5p, miR-34a-5p, miR-103a-3p, and miR-125a-5p were even reduced significantly in patient circulation (Fig. 2D). [score:1]
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These sequences, miR-1-5p, miR-146a-5p, miR-150-5p, miR-206, miR-342-3p, miR-574-5p, and miR-1283, had time- and dose-specific changes in abundance (Fig 6A). [score:1]
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01  hsa-let-7a-5p MIMAT0000062 0.010 −2.98  hsa-miR-4454 MIMAT0018976 0.021 −2.64  hsa-miR-148a-3p MIMAT0000243 0.030 −2.31  hsa-miR-146b-5p MIMAT0002809 0.009 −2.12  hsa-miR-342-3p MIMAT0000753 0.010 −2.11  hsa-let-7f-5p MIMAT0000067 0.021 −2.03  hsa-miR-26a-5p MIMAT0000082 0.034 −2.01  hsa-let-7d-5p MIMAT0000065 0.038 −2.01  hsa-miR-30b-5p MIMAT0000420 0.019 −1.96  hsa-miR-29b-3p MIMAT0000100 0.044 −1.94  hsa-miR-29a-3p MIMAT0000086 0.024 −1.70Significant deregulated microRNAs in JMML patients compared to Healthy Donors controls (P<0.05; see paragraph in Matherials and Methods section). [score:1]
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Port et al. showed that miR-342-3p was the candidate for prediction of hematologic ARS in baboons [29]. [score:1]
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