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52 publications mentioning hsa-mir-542

Open access articles that are associated with the species Homo sapiens and mention the gene name mir-542. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 255
It also inhibits growth of human lung cancer cells, perhaps by targeting EGFR mRNA [19] and is downregulated in thyroid tumors, suggesting miR-542-5p acts as a tumor suppressor in these cancers [20]. [score:10]
These results suggested that miR-542-5p downregulated HUWE1 expression by directly targeting its 3′UTR. [score:9]
Knockdown of HUWE1 by siRNA in osteosarcoma cells transfected with miR-542-5p inhibitors attenuated the suppressive effects of miR-542-5p inhibitor on the proliferation of osteosarcoma cells (Figure 6D, 6E). [score:8]
We identified nine upregulated (both of the iTRAQ ratios 115:114 > 1.5 and 117:116 > 1.5) and seven downregulated proteins (both of the iTRAQ ratios 115:114 < 0.67 and 117:115 < 0.67) after transfection with the miR-542-5p mimic. [score:7]
Results of cell cycle analysis revealed that overexpression of miR-542-5p resulted in a reduced G [2]/M population in MNNG/HOS and U2OS cells, whereas inhibition of miR-542-5p inhibited cell cycle progression, with increased numbers of cells in G [2]/M phase (Figure 3B, 3D). [score:7]
The relative expression of HUWE1, CSE1L and PTBP1 is shown in Supplementary Figure 4. Through the use of the bioinformatics tools, TargetScan, miRNAorg and miRwalk, HUWE1 was predicted to be the target gene of miR-542-5p. [score:7]
C. Heat map of upregulated and downregulated proteins in both MNNG/HOS and U2OS cells after transfection with miR-542-5p. [score:7]
Further investigation revealed that HUWE1 was a direct target of miR-542-5p, and that reduced expression of this protein played an important role in the tumor-promoting effect of miR-542-5p overexpression. [score:6]
A. B. of MNNG/HOS cells stably expressing the miR-542-5p mimic, miR-542-5p inhibitor or miR-control. [score:5]
Data from the present study showed that overexpression of miR-542-5p reduced levels of HUWE1, CSE1L and PTBP1, while inhibition of miR-542-5p increased levels of these proteins. [score:5]
Our findings suggest miR-542-5p enhances the growth of osteosarcoma cells by targeting HUWE1 and may provide a potentially useful therapeutic target for treatment of osteosarcoma. [score:5]
s showed that overexpression of miR-542-5p promoted colony formation and inhibition hindered colony formation (Figure 4A, 4B). [score:5]
To determine whether miR-542-5p reduced HUWE1 expression through direct binding to its 3′UTR, we constructed the 3′UTR fragment of HUWE1, and the corresponding mutant counterpart was inserted directly downstream of the firefly luciferase reporter gene (Figure 5F). [score:5]
Figure 4MiR-542-5p promotes the growth of osteosarcoma tumors in vivo A. B. of MNNG/HOS cells stably expressing the miR-542-5p mimic, miR-542-5p inhibitor or miR-control. [score:5]
1×10 [3] MNNG/HOS cells stably expressing the miR-542-5p mimic, miR-542-5p inhibitor or miR-control were seeded in 6-well plates. [score:5]
The data showed that overexpression of miR-542-5p reduced levels of HUWE1, CSE1L and PTBP1, and inhibition increased levels of HUWE1, CSE1L and PTBP1 in both cell lines (Figure 5D, 5E). [score:5]
Compared with non-tumor tissue, miR-542-5p expression was upregulated in osteosarcoma (Figure 7A). [score:5]
The results showed that upregulation of miR-542-5p promoted osteosarcoma cell proliferation; in contrast, knockdown of miR-542-5p had the opposite effect (Figure 3A, 3C). [score:5]
MNNG/HOS cells stably expressing the miR-542-5p mimic, the miR-542-5p inhibitor or the miR-control were subcutaneously injected into the left scapulas of nude mice, and the animals were closely monitored for tumor growth for 6 weeks. [score:5]
MNNG/HOS and U2OS cells were transiently transfected with a miR-542-5p mimic or inhibitor to increase or decrease expression of the miRNA. [score:5]
Moreover, miR-542-5p expression was upregulated in human osteosarcoma tissue compared with corresponding non-tumor tissues. [score:5]
Importantly, these findings indicate that miR-542-5p may be a promising new therapeutic target for suppression of osteosarcoma proliferation. [score:5]
MiR-542-5p promotes tumor formation in vivoMNNG/HOS cells stably expressing the miR-542-5p mimic, the miR-542-5p inhibitor or the miR-control were subcutaneously injected into the left scapulas of nude mice, and the animals were closely monitored for tumor growth for 6 weeks. [score:5]
MiR-542-5p promotes the proliferation of osteosarcoma cells in vitroMNNG/HOS and U2OS cells were transiently transfected with a miR-542-5p mimic or inhibitor to increase or decrease expression of the miRNA. [score:5]
MNNG/HOS cell lines stably expressing the miR-542-5p mimic, the miR-542-5p inhibitor or the miR-control were established. [score:5]
C. of HUWE1 expression in MNNG/HOS and U2OS cells after transfection with anti-miR-NC, miR-542-5p inhibitors and si-HUWE1. [score:5]
Conversely, miR-542-5p was upregulated in rectal cancer and basal cell carcinomas, indicating that miR-542-5p may act as an oncogene in those cancers [21, 22]. [score:4]
HUWE1 is the direct downstream target of miR-542-5p. [score:4]
Upregulation of miR-542-5p was also associated with EMT in human carcinosarcomas [23]. [score:4]
To verify the involvement of HUWE1 in the miR-542-5p -induced promotion of osteosarcoma cell proliferation, we knocked down endogenous HUWE1 expression in osteosarcoma cells using a specific siRNA. [score:4]
For tumor growth assays, MNNG/HOS cells stably expressing the miR-542-5p mimic, miR-542-5p inhibitor or miR-control were injected subcutaneously into the left scapulas of nude mice (6-week-old BALB/c-nu/nu, 6 per group, 2×10 [6] cells per mouse). [score:4]
s showed HUWE1 is a direct target of miR-542-5p in osteosarcoma. [score:4]
The miR-542-5p -mimic, miR-542-5p -inhibitor and miR-control lentiviral vectors were purchased from GenePharma (Shanghai, China). [score:3]
D. E. Representative western blots displaying the levels of HUWE1, CSE1L and PTBP1 proteins after transfection with miR-542-5p mimics or inhibitors. [score:3]
The results demonstrated that miR-542-5p -overexpressing tumors were significantly larger in size and volume compared with control tumors, whereas miR-542-5p-underexpressing tumors were smaller in size and volume compared with control tumors (Figure 4C, 4D). [score:3]
Kaplan-Meier analysis revealed a significant difference in disease free survival time between the high and low miR-542-5p groups. [score:3]
The sequences are as follows: miR-542-5p -mimic lentiviral vector (5′-TCGGGGATCATCATGTCACGAGA-3′); miR-542-5p -inhibitor lentiviral vector (5′-TCTCGTGACATGATGATCCCCGA-3′); miR-control lentiviral vector (5′-TTCTCCGAACGTGTCACGT-3′). [score:3]
Functional screening by in vitro transfection of miRNA mimics and inhibitorsMiRNA mimics for miR-1237, miR-365b-5p, miR-550a-5p and miR-135a-3p and miRNA inhibitors for miR-301b, miR-503, miR-542-5p and miR-210 were chosen for further functional investigation. [score:3]
The results showed that inhibition of miR-542-5p could restrain the proliferation of tumor cells, whereas the other miRNAs had no discernible effect on the proliferation of MNNG/HOS cells (Figure 2). [score:3]
Cell cycle changes were analyzed by flow cytometry after transfection with the miR-542-5p mimic or inhibitor. [score:3]
To identify the underlying mechanism by which miR-542-5p functions, in the present study iTRAQ combined with NanoLC-MS/MS analysis was used to identify the proteins differentially expressed after transfecting cells with a miR-542-5p mimic. [score:3]
A Kaplan-Meier analysis revealed a significant difference in disease free survival time between the high miR-542-5p group and low miR-542-5p group (χ2=4.193, P=0.041) (Figure 7B). [score:3]
iTRAQ combined with NanoLC−MS/MS analysis [11] was used to identify proteins that were differentially expressed after transfection with the miR-542-5p mimic. [score:3]
Stable expression of miR-542-5p using lentiviral vectors. [score:3]
We performed GO analysis and KEGG pathway analysis on the differentially expressed miRNAs, and the results are shown in Supplementary Figure 1. Ultimately, fifteen potential miRNAs associated with the proliferation of osteosarcoma were selected for microarray validation by quantitative real-time RT-PCR analysis, including miR-1237, miR-550a-5p, miR-365b-5p, miR-135a-3p, miR-933, miR-762, miR-629-3p, miR-542-5p, miR-503, miR-301b, miR-210, miR-374a-5p, miR-199a-5p, miR-199a-3p and miR-195-5p. [score:3]
C. The expression of HUWE1 was measured in the presence of low and high miR-542-5p expression levels. [score:3]
In conclusion, the results obtained in the present study indicate that overexpression of miR-542-5p promotes the proliferation of osteosarcoma in vitro and in vivo. [score:3]
We then transfected si-HUWE1 and miR-542-5p inhibitors together into MNNG/HOS and U2OS cells. [score:3]
iTRAQ, combined with NanoLC−MS/MS analysis, was used to identify proteins that were differentially expressed in MNNG/HOS and U2OS cells after transfection with the miR-542-5p mimic. [score:3]
Moreover, HUWE1 levels were negatively correlated with miR-542-5p expression in osteosarcoma tissues (Figure 7C). [score:3]
Further study showed that overexpression of miR-542-5p promoted tumorigenesis of osteosarcoma cells in vivo. [score:3]
MiR-542-5p expression is inversely correlated with levels of HUWE1 in osteosarcoma. [score:2]
D. CCK8 assays were determined after transduction with the miR-542-5p inhibitors, anti-miR-NC and si-HUWE1. [score:2]
F. Representative images and the table depict the results of cell cycle assays in MNNG/HOS and U2OS cells after transduction with the miR-542-5p inhibitors, anti-miR-NC and si-HUWE1. [score:2]
We used quantitative real-time PCR (qRT-PCR) to measure the expression of miR-542-5p in 40 pairs of human tissue samples; each pair comprised an osteosarcoma sample and a corresponding non-tumor tissue sample. [score:1]
These data indicate that miR-542-5p exhibits tumor-promoting activity in osteosarcoma and predicts poor patient prognosis. [score:1]
Statistical significance was observed between the wild type and the mutant groups transfected with miR-542-5p. [score:1]
MNNG/HOS and U2OS cells were transfected with the miR-542-5p mimic or with miR-NC for 48 h and harvested, and 100 μg of the MNNG/HOS cell lysates were labeled with iTRAQ labeling reagents 115 (miR-542-5p mimic) and 114 (miR-NC) (Applied Biosystems, Foster City, CA). [score:1]
HUWE1 is the critical mediator of miR-542-5p in osteosarcoma cells. [score:1]
F. The sequences of the putative miR-542-5p binding sites in wild type (emphasized with shadow) and mutant (red) HUWE1-3′UTR. [score:1]
A mixture of 50 ng pluc-3′UTR, 10 ng Renilla and 5 pmol miRNA-542-5p mimic or negative control were co -transfected into HEK-293T cells according to the recommended instructions using Lipofectamine 2000. [score:1]
Moreover, levels of miR-542-5p and HUWE1 are inversely correlated in osteosarcoma tissues. [score:1]
MiRNA mimics for miR-1237, miR-365b-5p, miR-550a-5p and miR-135a-3p and miRNA inhibitors for miR-301b, miR-503, miR-542-5p and miR-210 were chosen for further functional investigation. [score:1]
Effects of miR-542-5p on the proliferation and cell cycle progression of osteosarcoma cells. [score:1]
Our experimental data revealed that miR-542-5p promoted the proliferation of osteosarcoma cells, but did not influence metastasis. [score:1]
After functional screening, we found that miR-542-5p promoted proliferation in osteosarcoma cells. [score:1]
Notably, the function of miR-542-5p appears to vary in different tumors. [score:1]
B. The prognostic value of miR-542-5p for osteosarcoma patients assessed by Kaplan-Meier analysis. [score:1]
Similarly, whole-cell lysates from U2OS cells transfected with the miR-542-5p mimic or miR-NC were labeled with iTRAQ labeling reagents 117 and 116 (Applied Biosystems, Foster City, CA), respectively. [score:1]
G. The relative luciferase activity of luciferase reports with wild type or mutant HUWE1-3′UTR were determined in HEK 293T cells, which were co -transfected with the miR-542-5p mimic or miR-NC. [score:1]
Thus, miR-542-5p may enhance cell proliferation by promoting the G [2]/M phase transition. [score:1]
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2
[+] score: 166
To clarify whether inhibition of PRL and WNT4 expression was a direct effect of miR-542-3p or an indirect effect caused by IGFBP1 knockdown, we transfected primary cultures with either non -targeting small interfering RNA (siRNA) or siRNA targeting IGFBP1. [score:12]
We were able to demonstrate that miR-542-3p directly regulates IGFBP1 expression during HESCs and indirectly regulates the expression of other decidual marker genes, such as PRL and WNT4. [score:9]
IGFBP1 is a bona fide target of miR-542-3pTo examine if miR-542-3p targets IGFBP1 directly, a reporter construct was generated by inserting the putative binding site of miR-542-3p into the 3′ untranslated region (UTR) of the IGFBP1 gene downstream of a firefly luciferase reporter vector (IGFBP1-wt). [score:8]
To the best of our knowledge, the current report is the first to identify that miR-542-3p directly regulates morphological and biological differentiation of HESCs through targeting IGFBP1 expression. [score:7]
Compared with cells transfected with control miRNA mimic, the expression of miR-542-3p in response to 8-br-cAMP and MPA treatment was markedly up-regulated, approximately 2,200-fold, in cultures expressing miR-542-3p mimic (Fig. S3). [score:7]
Among the 1,205 sets of human miRNAs covered by the array, five (miR-503, miR-542-3p, miR-155, miR-145* and miR-424) were significantly down-regulated upon decidualization (<0.5-fold) (Table 1A), whereas a single miRNA (miR-483-3p) increased in expression (>2-fold) (Table 1B) in all three decidualizing primary HESC cultures (Fig. 1A and Table 1A and B). [score:6]
In conclusion, the present study demonstrates that the downregulation of miR-542-3p expression in HESCs is permissive for morphological and molecular differentiation of HESCs. [score:6]
To examine if miR-542-3p targets IGFBP1 directly, a reporter construct was generated by inserting the putative binding site of miR-542-3p into the 3′ untranslated region (UTR) of the IGFBP1 gene downstream of a firefly luciferase reporter vector (IGFBP1-wt). [score:6]
Transfection of HESCs with miR-542-3p inhibited PRL and WNT4 expression after 6 days of decidualization by 60–70%. [score:5]
Further, overexpression of miR-542-3p can inhibit cell growth and prevent tumour formation in vivo 15. [score:5]
Therefore, repression of PRL and WNT4 expression in decidualizing HESCs upon transfection with miR-542-3p mimic likely involves mechanisms other than the inhibition the auto/paracrine actions of IGFBP-1. Clearly, additional experiments are required to test this hypothesis. [score:5]
Taken together, the data confirms that miR-542-3p inhibits IGFBP1 expression by binding to its 3′ UTR. [score:5]
The miR-542-3p candidate targeting sequence of IGFBP1 gene (5′-GAUGAAAUAAUGUU CUGUCACG-3′, part of the NCBI RefSeq ID of NM_000596) and its mutated sequence (5′-GAUGAAAUAAUGUU UCUGUGAG-3′) were inserted downstream of the pGL4.13 luciferase expression vector (Promega Corporation, Madison, WI, USA). [score:5]
Further, Estella et al. found no significant change in the expression of miR-542-3p, which may be due to the differences in endometrial samples, decidualization protocol, or the expression profiling technique. [score:5]
Similar to miR-542-3p mimic transfection, IGFBP1 knockdown was sufficient to impair PRL and WNT4 expressions (Fig. 2C), suggesting that IGFBP-1 itself plays a role in regulating other decidual marker genes. [score:5]
IGFBP1 is a direct target of miR-542-3p. [score:4]
Effect of miR-542-3p overexpression or IGFBP-1 knockdown in decidualizing HESCs. [score:4]
Our results indicate that miR-542-3p plays an important role in endometrial decidualization, at least in part, by regulating IGFBP1 expression. [score:4]
Although the current study focused on miR-542-3p, other differentially expressed miRNAs, including miR-424, miR-503 and miR-155, may equally functionally regulate decidualization. [score:4]
This analysis identified six major induced decidual genes that were also putative targets of miR-542-3p, miR-424 or miR-503 (Table 2). [score:3]
IGFBP1 is a bona fide target of miR-542-3p. [score:3]
On the other hand, it has been reported that miR-542-3p is generally underexpressed in cancers arising from the colon, prostate and lung. [score:3]
We focused on miR-542-3p and its predicted target gene IGFBP1, a well-known decidual marker 4 12, for further analysis. [score:3]
Differential expression of miR-542-3p was confirmed by quantitative real-time polymerase chain reaction (qRT-PCR) analysis (Fig. 1B). [score:3]
Taken together, these results demonstrate that miR-542-3p is a potent inhibitor of HESC differentiation. [score:3]
To determine the functional significance of the loss of miR-542-3p expression in differentiating HESCs, primary cultures were transfected with either miR-542-3p mimic or negative control miRNA mimic prior to decidualization over a time course lasting 6 days. [score:3]
How to cite this article: Tochigi, H. et al. Loss of miR-542-3p enhances IGFBP-1 expression in decidualizing human endometrial stromal cells. [score:3]
On the other hand, Kureel et al. demonstrated that miR-542-3p suppresses osteogenic differentiation and promotes osteoblast apoptosis by repressing bone morphogenetic protein 7 and its downstream signalling 16. [score:3]
mirVana [TM] miRNA mimic (#MC11340; Applied Biosystems) for hsa-miR-542-3p or siRNA targeting IGFBP1 (Silencer select, s7225; Applied Biosystems) was mixed with Lipofectamine 2000 (Invitrogen), according to the manufacturer’s instructions, and added to HESCs in six-well culture plates at a density of 80–90% confluence. [score:3]
Decidualisation is inhibited by miR-542-3p. [score:3]
The IGFBP1-mut reporter was not significantly inhibited by miR-542-3p mimic. [score:3]
We then focused on miR-542-3p and its putative target IGFBP1, which encodes for the major decidual secretory protein 4 12. [score:3]
These observations suggest that miR-542-3p is a promising target for cancer therapy. [score:3]
qRT-PCR analysis of miR-542-3p and IGFBP1 mRNA expression in undifferentiated and differentiating HESCs in samples used for microarray experiments. [score:3]
To assess any potential toxicity of the miR-542-3p mimic transfection, apoptosis and necrosis were quantified by direct determination of nucleosomal DNA fragmentation using the Apoptotic/Necrotic/Healthy Cells Detection Kit (Takara bio Inc. [score:2]
Compared to cells transfected with control miRNA mimic, the induction of IGFBP1 transcripts in response to 8-br-cAMP and MPA treatment was markedly inhibited in cultures transfected with the miR-542-3p mimic (Fig. 2B). [score:2]
The expression level of miR-542-3p relative to U6 was calculated by the 2 [−ΔΔct] method 34. [score:1]
The mature sequences of hsa-miR-542-3p were 5′-UGUGACAGAUUG AUAACUGAAA-3′ (miRBase Accession number: MIMAT0003389). [score:1]
By contrast, morphological transformation was absent upon transfection of cells with miR-542-3p mimic. [score:1]
Those two vectors with an amount of 200 ng and a final concentration of 30 nM miR-542-3p mimic were co -transfected to HESCS treated with 0.5 mM 8-br-cAMP and 10 [−6] M MPA for 6 days before transfection. [score:1]
Similar to IGFBP1, the induction of PRL and WNT4 was repressed by miR-542-3p mimic (Fig. 2B). [score:1]
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3
[+] score: 135
While either miRZip-203 or miRZip-542-3p had little effect on entinostat -mediated reduction of Survivin, inhibition of both miR-203 and miR-542-3p attenuated entinostat's inhibitory effect on Survivin (Figure 6A), suggesting that miR-203 and miR-542-3p worked cooperatively in entinostat action to downregulate Survivin. [score:8]
Entinostat enhances expression of miR-203 (in vitro and in vivo) and miR-542-3p (in vitro) via inhibition of HDAC, downregulation of DNMT1, and/or other mechanisms to reduce Survivin, and thereby potentiate paclitaxel -induced apoptosis in NSCLC cells. [score:8]
Figure 12Entinostat enhances expression of miR-203 (in vitro and in vivo) and miR-542-3p (in vitro) via inhibition of HDAC, downregulation of DNMT1, and/or other mechanisms to reduce Survivin, and thereby potentiate paclitaxel -induced apoptosis in NSCLC cells. [score:8]
Taken together, our data indicate that both miR-203 and miR-542-3p contribute to entinostat -mediated reduction of Survivin; and upregulation of the two miRNAs is necessary and sufficient for entinostat potentiation of paclitaxel -induced growth inhibition and apoptosis in NSCLC cells. [score:6]
MiR-203 and/or miR-542-3p mimics specifically downregulate Survivin and significantly enhance paclitaxel -induced growth inhibition and apoptosis in NSCLC cells. [score:6]
As a consequence, simultaneous inhibition of miR-203 and miR-542-3p significantly reversed entinostat enhancement of paclitaxel -induced growth inhibition and apoptosis (Figure 6B–6D). [score:5]
Figure 11The expression levels of miR-203, but not miR-542-3p, are significantly increased, associated with miR-203 promoter hypermethylation, and inversely correlated with the expression of DNMT1 and Survivin in NSCLC tumors(A) The expression levels of miR-203 and miR-542-3p in NSCLC tumors and their self-paired normal adjacent lung tissues (n = 20) were measured by qRT-PCR and normalized to RNU6B. [score:5]
Lentiviral miRZip expression system (scramble control, miRZip-203, or miRZip-542-3p) was applied to fulfill specific inhibition of miR-203 or miR-542-3p in NSCLC cells. [score:5]
The expression levels of miR-203, but not miR-542-3p, are significantly increased, associated with miR-203 promoter hypermethylation, and inversely correlated with the expression of DNMT1 and Survivin in NSCLC tumors. [score:5]
These data suggest that 1) increased DNMT1 may not alter miR- 542-3p expression in NSCLC; 2) although miR-542-3p contributes to entinostat -induced growth inhibition and apoptosis in vitro, it has little effect on entinostat potentiation of paclitaxel efficacy in vivo. [score:5]
Recent studies show that a number of miRNAs, including miR-203 and miR-542-3p, play critical roles in regulating Survivin expression in cancer cells [45]. [score:4]
Entinostat downregulates Survivin via induction of miR-203 and miR-542-3p. [score:4]
In summary, we demonstrate that entinostat downregulates Survivin via induction of miR-203 and miR-542-3p in vitro and/or in vivo, and thereby potentiates paclitaxel -mediated antitumor activity against NSCLC. [score:4]
Specific knockdown of miR-203 and/or miR-542-3p reverses entinostat-enhanced paclitaxel -mediated growth inhibition and apoptosis in NSCLC cells. [score:4]
We then sought to understand if the induction of miR-203 and/or miR-542-3p was required for entinostat -induced downregulation of Survivin. [score:4]
Interestingly, entinostat significantly upregulated miR-203 (not miR-542-3p); and this induction was further enhanced when entinostat was combined with paclitaxel (Figure 7D). [score:4]
Entinostat selectively increases the expression levels of miR-203 and miR-542-3p in A549 and H460 cells. [score:3]
Statistics of the relative expression values of miR-203, miR-542-3p, Survivin, and DNMT1 in the self-paired clinical samples from patients with NSCLC. [score:3]
We next explored whether the induction of miR-203 and/or miR-542-3p was sufficient to inhibit Survivin. [score:3]
It seemed that miR-542-3p or two miRNA mimic(s) were more effective than miR-203 mimic to enhance paclitaxel -induced growth inhibition (Figure 5B). [score:3]
To test this hypothesis, we first examined the expression of miR-203 and miR-542-3p as well as Survivin and DNMT1 in 20 freshly-obtained NSCLC samples and their self-paired normal adjacent lung tissues (Table 1). [score:3]
There was no correlation between the expression of miR-542-3p and mRNA levels of either Survivin or DNMT1 (Figure 11A and 11D). [score:3]
It appeared that chemotherapy alone had no effect on the miRNAs in vitro, as treatment of A549 or H460 cells with paclitaxel did not alter the expression of either miR-203 or miR-542-3p (Data not shown). [score:3]
The lentiviral miRZip-203 or miRZip-542-3p was applied to specifically inhibit miR-203 or miR-542-3p, respectively. [score:3]
More importantly, a significant inverse correlation was detected between miR-203 (not miR-542-3p) and the expression of Survivin (r = −0.561, P = 0.01) or DNMT1 (r = −0.502, P = 0.024). [score:3]
Nonetheless, majority of the studies are carried out in preclinical mo dels, it is currently unknown whether the expression of miR-203 and/or miR-542-3p is altered in NSCLC tumors. [score:3]
Quantitative real-time (qRT)-PCR showed that entinostat significantly induced miR-203 and miR-542-3p, two Survivin -targeting miRNAs [27, 28], in a dose- and time -dependent manner (Figure 4). [score:3]
QRT-PCR analyses found that the expression levels of miR-203, but not miR-542-3p were significantly decreased in NSCLCs as compared to that in normal lung tissues (Figure 11A). [score:2]
Independent-samples t-test showed that the expression of miR-203, but not miR-542-3p, was significantly reduced in NSCLCs as compared to that in normal lung tissues (Table 2). [score:2]
NS, no significance Figure 5A549 and H460 cells were either mock transfected or transfected with miR-203 mimic (40 nmol/L), or miR-542-3p mimic (10 nmol/L), or combinations of two miRNA mimics. [score:1]
NS, no significance A549 and H460 cells were either mock transfected or transfected with miR-203 mimic (40 nmol/L), or miR-542-3p mimic (10 nmol/L), or combinations of two miRNA mimics. [score:1]
The HDACi entinostat selectively reduced Survivin via induction of miR-203 and miR-542-3p, and thereby significantly enhanced paclitaxel -induced apoptosis in NSCLC cells. [score:1]
While transfection with the mimic of either miR-203 or miR-542-3p slightly decreased Survivin, the combinations of both miRNA mimics profoundly reduced Survivin in A549 and H460 cells (Figure 5A). [score:1]
However, induction of miR-542-3p by entinostat was observed in vitro, not in vivo. [score:1]
The expression levels of miR-203, miR-542-3p, Let-7c, and miR-29b were measured by qRT-PCR. [score:1]
N) miR-203 methylation miR-542-3p (C vs. [score:1]
Hypermethylation of miR-203 promoter is associated with lower levels of miR-203 and higher levels of both DNMT1 and Survivin in NSCLC tumorsWe next focused our clinical studies on miR-203 and miR-542-3p. [score:1]
The relative mRNA abundance of miR-203, miR-542-3p, Survivin, and DNMT1, as well as the methylation status of miR-203 promoter in the clinical samples of NSCLC patients. [score:1]
NS, no significance Figure 5A549 and H460 cells were either mock transfected or transfected with miR-203 mimic (40 nmol/L), or miR-542-3p mimic (10 nmol/L), or combinations of two miRNA mimics. [score:1]
We next focused our clinical studies on miR-203 and miR-542-3p. [score:1]
The relative mRNA abundance of miR-203, miR-542-3p, Survivin, or DNMT1 was presented as 2 [^−ΔΔCt]. [score:1]
Clinical analysis found no difference of miR-542-3p levels between NSCLC tumors and the normal lung tissues. [score:1]
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4
[+] score: 25
The qRT-PCR results showed that three overexpressed microRNAs(miR-542-5p, miR-424, miR-30a) in hepatic differentiation was also overexpressed in osteogenic differentiation, one underexpressed microRNAs (miR-762)in hepatic differentiation was also underexpressed in osteogenic differentiation. [score:9]
Seven over-expressed microRNAs that were altered at least four fold, including hsa-miR-671-5p, hsa-miR-542-5p, hsa-miR-542-3p, hsa-miR-1185, hsa-miR-539, hsa-miR-148a and hsa-miR-301a, (Figure 4A) and six over-expressed microRNAs that were highly expressed (normalized data ≥6), including hsa-miR-1290, hsa-miR-136, hsa-miR-424, hsa-miR-30a, hsa-miR-148a and hsa-miR-1246 (Figure 4B), were selected for further qRT-PCR analyses. [score:7]
The qRT-PCR results demonstrated that the expression patterns of hsa-miR-542-5p, hsa-miR-542-3p, hsa-miR-148a, hsa-miR-1290, hsa-miR-424, hsa-miR-30a and hsa-miR-1246 were consistent with the microarray results (Figure 4C). [score:3]
The expression of miR-542-5p, miR-542-3p and miR-424 in both L02 and HepG2 cells was even lower than in hUC-MSCs. [score:3]
The expression of miR-542-5p increased in both the hepatic differentiation of hUC-MSCs and LDPCs [21]. [score:3]
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5
[+] score: 24
These results indicated that overexpression of the candidate miRNAs (miR-302c, miR-320a, miR542-3p, miR-641, miR-661 and miR-940) could, indeed, reduce the surface expression of MICB protein. [score:5]
Finally, we concluded that not only MICB expression was regulated by miR-320a and miR-940 but could also be controlled by other candidate miRNAs such as miR-302c, miR-542-3p, miR-641 and miR-661. [score:4]
The overexpressing miRNA mimic vectors (miR-302c, miR-320a, miR-542-3p, miR-641, miR-661 and miR-940 mimics) were transiently transfected into 293T cells and were co -transfected with luciferase reporter constructs containing wild-type 3-′UTR of MICB (pMICB_3U). [score:3]
Consequently, to confirm hypothesis of these studies we constructed plasmids to overexpress candidate miRNAs (miR-302c, miR-320a, miR-542-3p, miR-641, miR-661 and miR-940 mimic) and then these mimic miRNAs or control mimic plasmids were co -transfected with reporter construct containing wild-type 5′-UTR (pMICB_5U) into 293T cells. [score:3]
Thus, the candidate miRNAs (miR-302c, miR-320a, miR-542-3p, miR-641, miR-661 and miR-940) could regulate 5′-UTR of MICB by direct binding. [score:3]
Overexpression of candidate miRNAs in HeLa was performed by transfection with miRNA mimic vectors (miR-302c, miR-320a, miR542-3p, miR-641, miR-661 and miR-940) or control mimic vector. [score:3]
These results indicated that miRNA candidates (miR-320a, miR-542-3p, miR641, miR-940, miR-302c and miR-661) interacted with a predicted binding site on 3′-UTR of MICB. [score:1]
miR-542-3p and miR-940 have binding sites on the core promoter, initiator element (Inr) that has function similar to TATA in facilitating TATA binding protein or the transcription factor II D (TFIID) [40]. [score:1]
One type of constructs contained the mutated binding sites of both known miRNAs (miR-20a, miR-93 and miR-106b) and nine novel miRNAs (our candidate miRNAs, miR-320c, miR-320a, miR-320b, miR-320c, miR-320d, miR-542-3p, miR-641, miR-661 and miR-940) and another type contained only the mutated binding sites of known miRNAs as a positive control (Figure 3A). [score:1]
[1 to 20 of 9 sentences]
6
[+] score: 19
In order to further understand the role of aberrant miRNAs in physiological functions and biologic processes in arsenite -induced neoplastic transformation cells, 11 downregulated miRNAs (miR-197-3p, miR-192-5p, miR-127-3p, miR-139-5p, miR-490-3p, miR-196b-5p, miR-125a-3p, miR-298, miR-542-3p, miR-15b-5p, and miR-33b-5p) and six upregulated miRNAs (miR-200b-3p, miR-106b-5p, miR-574-5p, miR-320d, miR-200c-3p, and miR-141-3p) (Table S2) were selected, and their target genes were predicted with the TargetMiner, miRDB, and TarBase databases. [score:11]
Among the 191 dysregulated miRNAs, seventeen miRNAs (downregulation miRNAs: miR-197-3p, miR-192-5p, miR-127-3p, miR-139-5p, miR-490-3p, miR-196b-5p, miR-125a-3p, miR-298, miR-542-3p, miR-15b-5p, miR-33b-5p; upregulation miRNAs: miR-200b-3p, miR-106b-5p, miR-574-5p, miR-320d, miR-200c-3p, miR-141-3p, Table S2) were selected for bioinformatics analysis. [score:8]
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7
[+] score: 16
Furthermore, 3 of these candidates (miR-135b, miR-542-5p, and miR-652) had no expression in tumor samples and osteosarcoma cell lines, which minimizes the likelihood that expression differences are a result of differences between immortalized cell lines and heterogeneous tumor samples. [score:5]
Recently, a group has reported the association of miR-542-5p overexpression in favorable histology, MYCN nonamplified neuroblastoma samples [26, 27]. [score:3]
The two other microRNAs that were overexpressed and confirmed in this study, miR-542-5p and miR-652, have only a few reports in the literature. [score:3]
Using this strategy, we were able to identify twenty-two differentially expressed microRNAs, and 4 (miR-135b, miR-150, miR-542-5p and miR-652) were selected for individual confirmations. [score:3]
Of the 22 miRNAs initially identified, 4 were selected for individual confirmation (miR-135b, miR-150, miR-542-5p and miR-652) based upon the fact that they were differentially expressed in both comparisons of human tumor and osteosarcoma cell lines when compared to osteoblasts. [score:2]
[1 to 20 of 5 sentences]
8
[+] score: 16
[179] In addition, some non-BMP-regulated miRNAs also have regulatory roles in BMP signaling: miR-141 and -200a remarkably modulate the BMP-2 -induced pre-osteoblast differentiation through the translational repression of Dlx5; [180] miR-542-3p targets BMP7 and represses BMP7 -induced osteoblast differentiation and survival; [181] miR-20a promotes osteogenic differentiation through upregulation of BMP/Runx2 signaling by targeting PPARγ, Bambi, and Crim1; [182] miR-140 targets a mild inhibitor of BMP Dnpep, and loss of miR-140 in mice causes growth defects of endochondral bones and craniofacial deformities. [score:16]
[1 to 20 of 1 sentences]
9
[+] score: 15
Previously, we identified several tumor-suppressive miRNAs that are repressed in c-Src–transformed cells: miR-99a targets mTOR to suppress tumor progression, and miR-542-3p targets ILK to suppress tumor malignancy [32, 38]. [score:11]
Furthermore, it is possible that upregulation of ILK by repression of miR-542-3p also contributes to the activation of invasive potential induced via the miR-424/503–Rictor pathway. [score:4]
[1 to 20 of 2 sentences]
10
[+] score: 14
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-342, 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-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
The ectopic expression of miR-342-5p, miR-373 or miR-542-5p suppresses Enterovirus replication, but miR-10* facilitates CVB3 replication. [score:5]
Both miR-373 and miR-542-5p target the 5′ untranslated region (5′ UTR) of EV71 vRNA and thus attenuate viral propagation as assayed in RD cells (Figure 2) [100]. [score:4]
Similarly, miR-373 and miR-542-5p attenuate EV71 propagation by targeting the 5′ UTR of EV71 vRNAs. [score:3]
Yang Z. Tien P. MiR373 and miR542-5p regulate the replication of enterovirus 71 in rhabdomyosarcoma cells Chin. [score:2]
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11
[+] score: 13
B/ Depicted is the log [2 ] fc over time of the interpolated expression data of selected TFs that are predicted to regulate/miR-542. [score:4]
C/ Depicted is the log [2 ] fc over time of the interpolated expression data of, miR-542-3p, and miR-542-5p. [score:3]
Figure 4 shows that mir-424 and mir-542 are regulated by the same TFs and are thus as well clustered in the heat-map. [score:2]
A/ Depicted are the predicted regulations of/miR-542/miR-503 and their involvement in the monocytic differentiation. [score:2]
These pre-miRNAs form the mature miRNAs, miR-503, miR-542-5p, and miR-542-3p. [score:1]
Furthermore, the pre-mir-424 is transcribed together with pre-mir-503 and pre-mir-542 as one transcript. [score:1]
[1 to 20 of 6 sentences]
12
[+] score: 13
Exosomal mRNAs and miRNAs derived from tumor cells were recovered in lymph node stroma and lung fibroblasts, and were shown to significantly affect mRNA translation in the target cells, exemplified by abundant recovery of exosomal miR-494 and miR-542-3p, which targeted cadherin17 [89]. [score:7]
Althoff K, Lindner S, Odersky A, Mestdagh P, Beckers A, Karczewski S, et al. : miR-542-3p exerts tumor suppressive functions in neuroblastoma by downregulating Survivin. [score:6]
[1 to 20 of 2 sentences]
13
[+] score: 12
92) 43 hsa-mir-302a dbDEMC 19 hsa-let-7g dbDEMC, miR2Disease 44 hsa-mir-212 literature 20 hsa-let-7b dbDEMC, HMDD, miR2Disease 45 hsa-mir-372 dbDEMC 21 hsa-mir-150 dbDEMC, literature 46 hsa-mir-197 dbDEMC 22 hsa-mir-338 dbDEMC 47 hsa-mir-124 literature 23 hsa-mir-103 dbDEMC, miR2Disease 48 hsa-mir-378 HMDD 24 hsa-mir-15b dbDEMC, HMDD 49 hsa-mir-26b dbDEMC, miR2Disease 25 hsa-mir-31 dbDEMC, HMDD, miR2Disease 50 hsa-mir-542 higher RWRMDA (No. [score:11]
Hsa-mir-18a, hsa-mir-18b, hsa-mir-499, and hsa-mir-542 are ranked No. [score:1]
[1 to 20 of 2 sentences]
14
[+] score: 10
Evidence of the concerted interplay of miRNAs regulated by CpG-ODN and their potential target mRNAs was observed (Fig. 4) for 2 miRNAs upregulated (hsa-miR-302b and hsa-miR-374b) and for 13 miRNAs downregulated in CpG-ODN -treated mice (hsa-miR-135a, hsa-miR-136, hsa-miR-340, hsa-miR-445-5p, hsa-miR-424, hsa-miR-96, hsa-miR-142-3p, hsa-miR-140-5p, hsa-miR-542-3p, hsa-miR-18a, hsa-miR-18b, hsa-miR-101, and hsa-miR-99a). [score:10]
[1 to 20 of 1 sentences]
15
[+] score: 10
The choice of miRNAs for validation with real-time RT-PCR was based on their differential expression among the groups as well as their putative biological significance: miR-542-5p is predicted to target estrogen receptor alpha mRNA; miR-200a and miR-429 are both members of the miR-200 family; and miR-503 is the most down-regulated miRNA in both types of carcinoma and the precursor lesion. [score:8]
1 −2.0 −4.2 miR-410 −2.4 −1.7 −4.2 miR-424 −4.1 −2.6 −10.7 miR-424* −1.2 −4.0 −4.9 miR-431 2.2 −4.3 −1.9 miR-432 −1.9 −2.4 −4.6 miR-503 −8.6 −3.2 −27.3 miR-542-3p −3.2 −2.1 −6.9 miR-542-5p −2.0 −3.1 −6.1 miR-596 2.2 −4.4 −2.0 miR-610 1.9 −5.1 −2. [score:1]
Specific kits used were as follows: miR-542-5p: ABI#002240; miR-200a: ABI#000502; miR-429: ABI#001024; miR-503: ABI#001048. [score:1]
[1 to 20 of 3 sentences]
16
[+] score: 9
Several groups identified miR-542-5p as a putative tumor suppressor, whose expression has a prognostic value and might be important in NB tumor biology [120– 122]. [score:5]
Of note, miR-542-5p is predicted to target TBR1, a gene essential for proper development of neurons. [score:4]
[1 to 20 of 2 sentences]
17
[+] score: 9
For example, the levels of miR-542-3p are lower in decidualizing versus normal human ESCs, and overexpression of miR-542-3p inhibits the expression of IGFBP1, PRL, and WNT4, suggesting an inhibitory role of miR-542-3p in decidualization [94]. [score:9]
[1 to 20 of 1 sentences]
18
[+] score: 8
9 −3.8 hsa-miR-424 −4.2 −2 −4.5 hsa-miR-24-1* −3.9 −2.3 −4.1 hsa-miR-542-3p −2.9 −2.2 −3.8 hsa-miR-29b −2.6 −2.1 −3.3 hsa-miR-301a −2.4 −1.8 −2 hsa-miR-107 −2 −1.7 −2.2 hsa-miR-101 −1.8 −1.9 −1.8 hsa-miR-188-5p −1.7 −1.6 −1.8 Based on the 3 lists of DEMs, we focused our attention on the miRNAs whose expression was influenced specifically by the oncogenic alteration of AKT1, PIK3CA or PTEN, and, alternatively, on those commonly deregulated by two or three of the above-mentioned alterations. [score:4]
9 −3.8 hsa-miR-424 −4.2 −2 −4.5 hsa-miR-24-1* −3.9 −2.3 −4.1 hsa-miR-542-3p −2.9 −2.2 −3.8 hsa-miR-29b −2.6 −2.1 −3.3 hsa-miR-301a −2.4 −1.8 −2 hsa-miR-107 −2 −1.7 −2.2 hsa-miR-101 −1.8 −1.9 −1.8 hsa-miR-188-5p −1.7 −1.6 −1.8Based on the 3 lists of DEMs, we focused our attention on the miRNAs whose expression was influenced specifically by the oncogenic alteration of AKT1, PIK3CA or PTEN, and, alternatively, on those commonly deregulated by two or three of the above-mentioned alterations. [score:4]
[1 to 20 of 2 sentences]
19
[+] score: 8
77 × 10 [−05] miR-542-5p −3.591.58 × 10 [−05] miR-758 −2.578.54 × 10 [−06] miR-377 −2.531.07 × 10 [−05] miR-337-5p −2.196.91 × 10 [−05] In the former studies, four miRNAs (miR-182, miR-183, miR-200a and miR-200c) were found to be up-regulated in four of the six surveys. [score:4]
77 × 10 [−05] miR-542-5p −3.591.58 × 10 [−05] miR-758 −2.578.54 × 10 [−06] miR-377 −2.531.07 × 10 [−05] miR-337-5p −2.196.91 × 10 [−05] In the former studies, four miRNAs (miR-182, miR-183, miR-200a and miR-200c) were found to be up-regulated in four of the six surveys. [score:4]
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20
[+] score: 7
miR-424, miR-542-3p, and miR-454 were the most upregulated, and miR-494, miR-490-5p, and miR-486-5p were the most downregulated miRNAs in tumor in comparison to the normal tissue (28). [score:7]
[1 to 20 of 1 sentences]
21
[+] score: 7
Other miRNAs from this paper: mmu-mir-542
C-Src upregulation was correlated with miR-542-3p downregulation. [score:7]
[1 to 20 of 1 sentences]
22
[+] score: 7
Other miRNAs from this paper: hsa-let-7c, hsa-let-7d, hsa-mir-16-1, hsa-mir-21, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-28, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-99a, hsa-mir-101-1, hsa-mir-16-2, mmu-let-7g, mmu-let-7i, mmu-mir-27b, mmu-mir-30a, mmu-mir-99a, mmu-mir-101a, mmu-mir-125b-2, mmu-mir-126a, mmu-mir-128-1, mmu-mir-9-2, mmu-mir-142a, mmu-mir-144, mmu-mir-145a, mmu-mir-151, mmu-mir-152, mmu-mir-185, mmu-mir-186, mmu-mir-24-1, mmu-mir-203, mmu-mir-205, hsa-mir-148a, hsa-mir-34a, hsa-mir-203a, hsa-mir-205, hsa-mir-210, hsa-mir-221, mmu-mir-301a, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-27b, hsa-mir-125b-1, hsa-mir-128-1, hsa-mir-142, hsa-mir-144, hsa-mir-145, hsa-mir-152, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125b-2, hsa-mir-126, hsa-mir-185, hsa-mir-186, mmu-mir-148a, mmu-mir-200a, mmu-let-7c-1, mmu-let-7c-2, mmu-mir-16-1, mmu-mir-16-2, mmu-mir-21a, mmu-mir-24-2, mmu-mir-29a, mmu-mir-31, mmu-mir-34a, mmu-mir-148b, mmu-mir-339, mmu-mir-101b, mmu-mir-28a, mmu-mir-210, mmu-mir-221, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-125b-1, mmu-mir-128-2, hsa-mir-128-2, hsa-mir-200a, hsa-mir-101-2, hsa-mir-301a, hsa-mir-151a, hsa-mir-148b, hsa-mir-339, hsa-mir-335, mmu-mir-335, hsa-mir-449a, mmu-mir-449a, hsa-mir-450a-1, mmu-mir-450a-1, hsa-mir-486-1, hsa-mir-146b, hsa-mir-450a-2, hsa-mir-503, mmu-mir-486a, mmu-mir-542, mmu-mir-450a-2, mmu-mir-503, hsa-mir-151b, mmu-mir-301b, mmu-mir-146b, mmu-mir-708, hsa-mir-708, hsa-mir-301b, hsa-mir-1246, hsa-mir-1277, hsa-mir-1307, hsa-mir-2115, mmu-mir-486b, mmu-mir-28c, mmu-mir-101c, mmu-mir-28b, hsa-mir-203b, hsa-mir-5680, hsa-mir-5681a, mmu-mir-145b, mmu-mir-21b, mmu-mir-21c, hsa-mir-486-2, mmu-mir-126b, mmu-mir-142b, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
In the metastatic line, the miR-542 showed up-regulation of the 3p arm but down-regulation of the 5p arm. [score:7]
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23
[+] score: 7
As shown in the heat map, compared with sample on PID 0, most miRNAs were down-regulated in sample on PID 4, whereas only few miRNAs were differentially expressed in sample on PID 7. Compared with sample on PID 4, a majority of miRNAs were up-regulated in sample on PID 7. To validate the Solexa sequencing results, qRT-PCR was performed separately to investigate the relative expression levels of 5 randomly selected DE miRNAs (ssc-miR-424-3p, ssc-miR-542-5p, ssc-miR-365-5p, ssc-miR-450b-5p, ssc-miR-450a). [score:7]
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24
[+] score: 7
Furthermore, we found 8 miRNAs (miR-95, miR-139, miR-379, miR-429, miR-509, miR-518e, miR-542-5p, and miR-659) downregulated in both 6 h aDCs and tDCs with respect to iDCs. [score:4]
Interestingly, 5 miRNAs (miR-95, miR-429, miR-509, miR-542, and miR-659) were downregulated in tDCs and aDCs compared with iDCs. [score:3]
[1 to 20 of 2 sentences]
25
[+] score: 6
revealed that miR-221, miR-222, miR-210, miR-542-5p, miR-96, miR-182, and miR-143 are the miRNAs that can positively explain the gene activity profile; this means that increasing expression level of miRNAs will lead to increasing the transcription of activity centers. [score:3]
They all indicate the significant role of specific miRNAs (miR-221, miR-222, miR-210, miR-542-5p, miR-96, miR-182, and miR-143) in prostate cancer. [score:1]
The results emphasized the role of some miRNAs already validated in prostate cancer (miR-221, miR-222, mir-96 and mir-143), and identified novel miRNAs like miR-210, miR-542, miR-128 and miR-219 that do not have a known mode of action in prostate cancer. [score:1]
Other predicted miRNAs (miR-143, miR-542) may play a role in zinc homeostasis, focal adhesion, and cytoskeleton organization. [score:1]
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26
[+] score: 6
The expression of miR-23a, miR-181c, miR-192, miR-194, miR-208, miR-337-5p, miR-338-3p, miR-502-5p, miR-542-3p, miR-628-5p, and miR-672 is upregulated in the oral mucosa of heavy smokers with lung cancer versus patients without cancer and light smokers [66]. [score:6]
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27
[+] score: 6
In particular, miR-494 and miR-542-3p modulated the expression of cadherin-17 with concomitant upregulation of matrix metalloproteinases. [score:6]
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28
[+] score: 5
The same expression pattern was observed for miRNAs located near the studied loci (miR-424, miR-450a, miR-450b-5p, miR-503 and miR-542-3p). [score:3]
Furthermore, using the normal tissue panel, we observed a significant positive correlation between MIR503HG and LINC00629 lincRNAs (Fig 3K), and also between both lincRNAs and the neighboring miRNAs: miR-424, miR450a, miR-450b-5p, miR-542-3p and miR-503 (Fig 3A–3J). [score:1]
002207), miR-542-3p (Catalog No. [score:1]
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29
[+] score: 5
Conversely, miR-335 suppressed invasion through the TGF-β pathway [16], and miR-9 and miR-542-5p over -expression in human NB primary tumors associated to a better survival [12, 18, 23], making unlikely a positive role in the human metastatic process. [score:5]
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30
[+] score: 5
Finally, when miRNA expression pattern was linked to the cause of HCC, we found that the expression level of miR-181d, miR-542-3p, and miR-519e in HCC derived from CH was significantly higher than in HCC from liver cirrhosis (LC). [score:5]
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31
[+] score: 5
Other miRNAs from this paper: hsa-mir-199a-1, hsa-mir-199a-2, hsa-mir-184
In addition, microRNAs such as microRNA-542-3p, microRNA-184, and microRNA-199a-5p could target FZD7 and suppress cell proliferation [24– 26]. [score:5]
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32
[+] score: 5
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-16-1, hsa-mir-17, hsa-mir-21, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-30a, hsa-mir-31, hsa-mir-96, hsa-mir-99a, hsa-mir-16-2, hsa-mir-30c-2, hsa-mir-30d, hsa-mir-182, hsa-mir-183, hsa-mir-211, hsa-mir-217, hsa-mir-218-1, hsa-mir-218-2, hsa-mir-221, hsa-mir-222, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-23b, hsa-mir-30b, hsa-mir-125b-1, hsa-mir-132, hsa-mir-143, hsa-mir-145, hsa-mir-191, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-184, hsa-mir-190a, hsa-mir-195, rno-mir-322-1, rno-let-7d, rno-mir-335, rno-mir-342, rno-mir-135b, hsa-mir-30c-1, hsa-mir-299, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-379, hsa-mir-382, hsa-mir-342, hsa-mir-135b, hsa-mir-335, rno-let-7a-1, rno-let-7a-2, rno-let-7b, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7f-1, rno-let-7f-2, rno-let-7i, rno-mir-15b, rno-mir-16, rno-mir-17-1, rno-mir-21, rno-mir-23a, rno-mir-23b, rno-mir-24-1, rno-mir-24-2, rno-mir-25, rno-mir-26a, rno-mir-26b, rno-mir-30c-1, rno-mir-30e, rno-mir-30b, rno-mir-30d, rno-mir-30a, rno-mir-30c-2, rno-mir-31a, rno-mir-96, rno-mir-99a, rno-mir-125a, rno-mir-125b-1, rno-mir-125b-2, rno-mir-126a, rno-mir-132, rno-mir-143, rno-mir-145, rno-mir-183, rno-mir-184, rno-mir-190a-1, rno-mir-191a, rno-mir-195, rno-mir-211, rno-mir-217, rno-mir-218a-2, rno-mir-218a-1, rno-mir-221, rno-mir-222, rno-mir-299a, hsa-mir-384, hsa-mir-20b, hsa-mir-409, hsa-mir-412, hsa-mir-489, hsa-mir-494, rno-mir-489, rno-mir-412, rno-mir-543, rno-mir-542-1, rno-mir-379, rno-mir-494, rno-mir-382, rno-mir-409a, rno-mir-20b, hsa-mir-770, hsa-mir-190b, hsa-mir-543, rno-mir-466c, rno-mir-17-2, rno-mir-182, rno-mir-190b, rno-mir-384, rno-mir-673, rno-mir-674, rno-mir-770, rno-mir-31b, rno-mir-191b, rno-mir-299b, rno-mir-218b, rno-mir-126b, rno-mir-409b, rno-let-7g, rno-mir-190a-2, rno-mir-322-2, rno-mir-542-2, rno-mir-542-3
Differential expression of miR-23a, miR-23b,miR-542–3p, miR-211, and miR-17–5p in granulosa/cumulus cells from women undergoing assisted reproduction suggests aberrant miRNA expression may be an underlying etiology in female infertility [16, 17]. [score:5]
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For example, the miR-424-503 polycistron, miR-542-5p and 3p, and miR-450, all of which are likely to be part of the same primary transcript [8], are up-regulated significantly in senescent BJ cells. [score:4]
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Six miRNAs of them (miR-450b-5p, miR-424, miR-503, miR-542-3p, miR-629, and miR-214) were significantly underexpressed, while one miRNA (miR-592) was significantly overexpressed in NFA compared to normal pituitary tissues. [score:4]
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[+] score: 3
In vitro experiments have demonstrated that hyaluronic acid-decorated polymeric nanoparticles can co- deliver doxorubicin and miR-542-3p to breast cancer cell lines 33 and mesoporous silica nanoparticles have been exploited to simultaneously deliver a miR-122 antagomir and small molecule inhibitors to hepatocellular carcinoma cells 34. [score:3]
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[+] score: 3
The resistant haplotypes had differentially expressed miR-21-3p, miR-134-5p, miR-542-5p, and miR-671 these miRs were found to be associated with NFκβ pathway and increased resistance to infection suggesting their role in inflammation, though further functional analysis needs to be undertaken (Jiang et al., 2016). [score:3]
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[+] score: 3
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-17, hsa-mir-19a, hsa-mir-21, hsa-mir-31, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-105-1, hsa-mir-105-2, hsa-mir-199a-1, hsa-mir-34a, hsa-mir-187, hsa-mir-199a-2, hsa-mir-205, hsa-mir-214, hsa-mir-221, hsa-let-7g, hsa-let-7i, hsa-mir-128-1, hsa-mir-141, hsa-mir-144, hsa-mir-145, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-146a, hsa-mir-200c, hsa-mir-128-2, hsa-mir-29c, hsa-mir-376a-1, hsa-mir-378a, hsa-mir-133b, hsa-mir-429, hsa-mir-487a, hsa-mir-515-1, hsa-mir-515-2, hsa-mir-526b, hsa-mir-514a-1, hsa-mir-514a-2, hsa-mir-514a-3, hsa-mir-376a-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-656, hsa-mir-378d-2, 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-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-1275, hsa-mir-548p, hsa-mir-548i-1, hsa-mir-548i-2, hsa-mir-548i-3, hsa-mir-548i-4, hsa-mir-2114, hsa-mir-548q, hsa-mir-548s, hsa-mir-378b, hsa-mir-548t, hsa-mir-548u, hsa-mir-548v, hsa-mir-548w, hsa-mir-548x, hsa-mir-514b, hsa-mir-378c, hsa-mir-4303, hsa-mir-4309, hsa-mir-4307, hsa-mir-4278, hsa-mir-548y, hsa-mir-548z, hsa-mir-548aa-1, hsa-mir-548aa-2, hsa-mir-548o-2, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-548h-5, hsa-mir-548ab, hsa-mir-378f, hsa-mir-378g, 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-378h, hsa-mir-548ai, hsa-mir-548aj-1, hsa-mir-548aj-2, hsa-mir-548x-2, hsa-mir-548ak, hsa-mir-548al, hsa-mir-378i, hsa-mir-548am, hsa-mir-548an, 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-378j, hsa-mir-548ay, hsa-mir-548az, hsa-mir-548ba, hsa-mir-548bb, hsa-mir-548bc
However, only eight aberrantly expressed miRNAs (including has-miRplus-A1087, has-miR-542-3p, has-miR-141, has-miR-200c, has-miR-214, has-miR-29c, has-miR-378, and has-miR-128) were consistent with our findings. [score:3]
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[+] score: 3
Eight hsa-miRNAs underwent validation in the discovery samples by qPCR (miR-675-5p, miR-30c-1-3p, miR-483-5p, miR-542-5p, miR-142-3p, miR-223-3p, miR-32-3p, and miR-320a) according to the following criteria: available Exiqon probes, the best hits in bone array (signal intensity and significant differences between the groups), and predicted to target genes involved in bone metabolism. [score:3]
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[+] score: 3
In addition, changes were observed between the corpus and cauda regions with miR-200b, miR-10a, miR-424, miR-542, miR-31, miR-183 and miR-363 being significantly over-expressed in the corpus versus the cauda region (Fig. 2 B). [score:3]
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[+] 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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01 Stress response, cell proliferation miR-542 ↓2.60 NA miR-574 ↑2.09 Inflammation (Tlr9 activation), cell proliferation, apoptosis miR-669j ↑3.12 NA miR-672 ↑2.40 NA miR-674 ↑2.19 NA miR-744 ↑4.35Oncogene (Tgf) suppression miR-873 ↑2.53 ↑3.22 NA miR-1930 ↑3.31 NA miR-1934 ↑2.17 ↑3.27 NA miR-1942 ↑2.49 NA miR-3064 ↑2.50 NA miR-3065 ↑3.20 NA miR-3069 ↑2.98 NA miR-3071 ↑3.51 NA miR-3073 ↓2.78 NA miR-3092 ↑3.48 NA miR-3093 ↑3.28 NA miR-3109 ↓2.07 NAAll reported variations were statistically significant (P < 0.05). [score:3]
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As the presence of micro -RNAs that may downregulate PTGS2, such as miR-542-3p, was not evaluated in MCF-7 or HEK293FT cells, it is possible that this post-transcriptional regulation was not fully operational in the cell mo dels. [score:3]
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[+] score: 3
In our recent work, we demonstrated that the circulating miRNAs, miR-646, miR-141* and miR-542-3p were differentially expressed in the serum of cervical squamous cell carcinoma (SCC) patients before and after surgery, thus could potentially serve as non-invasive biomarkers and post-therapeutic monitors for cervical SCC [32]. [score:3]
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[+] score: 2
The effect of co- delivery of doxorubicin and miR-542-3p using hyaluronic acid decorated PEI-PLGA nanoparticle against breast cancer was studied [184]. [score:1]
Wang S Zhang J Wang Y Chen M Hyaluronic acid-coated PEI-PLGA nanoparticles mediated co- delivery of doxorubicin and miR-542-3p for triple negative breast cancer therapyNanomed Nanotechnol Biol Med. [score:1]
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Twenty of the 26 miRNAs belonged exclusively to the sporadic DT group, 5 miRNAs (miR-409-3p, miR-601, miR-542-5p, miR-487b and miR-4707-5p) were present in both tumor types, while miR-497-5p was detected only in Gardner's syndrome samples (Figure 1A and 1B). [score:1]
Five out the 101 miRNAs (miR-409-3p, miR-487b, miR-601, miR-542-5p and miR-4707-5p) were shared by both tumor types, 3 miRNAs (miR-320e, miR-497-5p and miR-2276) were specific to FAP -associated DTs and 93 were specific for sporadic DTs. [score:1]
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[+] score: 2
Mir-542-5p on the other hand, shows consistently low expression at prenatal time points, spikes at earliest childhood time point, then declines. [score:2]
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[+] score: 2
Six of the miRNAs identified as highly significant to tumors (HS-29, miR-135b, miR-32, miR-33, miR-542-5p and miR-96) displayed higher expression in pMMR stage IV as compared to stage II tumors (p < 0.05 and fold change > 1.5) (Figure 3C). [score:2]
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Besides the abovementioned miRNAs promoting myoblast differentiation, a few identified molecules such as miR-29b [49], miR-31 [50], miR-9 [51], miR-145 [52], miR-194 [53], miR-378 [54], miR-449 [55], miR-503 [11, 27], miR-542, [56], and miR-660 [11] were described in the literature as skeletal muscle-related. [score:1]
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severe (p<0.05) cfa-let-7a, cfa-let-7b, cfa-let-7c, cfa-let-7f, cfa-miR-127, cfa-miR-1271, cfa-miR-130a, cfa-miR-139, cfa-miR-17, cfa-miR-1836, cfa-miR-1837, cfa-miR-20a, cfa-miR-23a, cfa-miR-25, cfa-miR-26a, cfa-miR-29b, cfa-miR-378, cfa-miR-421, cfa-miR-502, cfa-miR-503, cfa-miR-542, cfa- miR-652, cfa-miR-653, cfa-miR-872 Normal and mild vs. [score:1]
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Taken together, these elements may represent a multipart transcript, and interestingly four additional miRNA coding sites (mir-542, mir-450a-2, mir-450a-1, and mir-450b) reside nearby, which do not have any evidence of being transcribed based on known dbEST sequence records. [score:1]
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For example, Hamrick et al., (2010) reported that miR-7, miR-468, miR-542, and miR-698 levels in mouse muscle tissue substantially increased with age, whereas miR-124a, miR-181a, miR-221, miR-382, miR-434, and miR-455 levels substantially decreased with age. [score:1]
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The 12 miRNAs (miR-23b, miR-25, miR-27b, miR-93, miR-106b, miR-189, miR-489, miR-505, miR-542-5p, miR-565, miR-652, and let-7d) were transfected into MCF7-ADR-Luc cells (Figure 4F). [score:1]
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