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11 publications mentioning hsa-mir-942

Open access articles that are associated with the species Homo sapiens and mention the gene name mir-942. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 195
We found that decreased expression level of miR-942 correlates with AKT knockdown and ISG12a expression is restored after AKT downregulation. [score:9]
When we used AKT inhibitor to block AKT activation, miR-942 was downregulated and ISG12a was upregulated (Supplementary Fig. S5A-C). [score:9]
First, after AKT knockdown, miR-942 expression was downregulated (Fig. 7B). [score:7]
In vitro and in vivo experiments revealed that elevated level of miR-942 in TRAIL-resistant cells or aggressive cancer tissues correlates with ISG12a downregulation, suggesting that miR-942 might be a causal factor in the downregulation of ISG12a in cancers. [score:7]
Our data demonstrated that miR-942 is significantly upregulated in TRAIL-resistant cells or aggressive cancer tissues, verse TRAIL-sensitive cells or less invasive cancer tissue, clearly indicating that miR-942 overexpression is a prerequisite of TRAIL-resistant HCC and gastric cancer cells. [score:6]
Conversely, knockdown of miR-942 expression by anti-miR-942 restored the expression of ISG12a in resistant BGC-823 cells and sensitized the cells to TRAIL -induced apoptosis (Supplementary Fig. S4B). [score:6]
Conversely, knockdown of miR-942 expression by anti-miR-942 in Huh7 cells, which was confirmed by real-time PCR, restored the expression of ISG12a in resistant cells (Fig. 6C) and sensitized the cells to TRAIL -induced apoptosis (Fig. 6D). [score:6]
Furthermore, we found an inverse correlation between miR-942 expression and ISG12a expression in cancer cell lines analyzed (Fig. 2C and Fig. 4C). [score:5]
To test whether miR-942 affects ISG12a expression, we examined the effect of miR-942 forced expression on ISG12a level in LH86 cells. [score:5]
To examine the effect of miR-942 forced expression on the expression of ISG12a and TRAIL sensitivity in cancer cells, we delivered pcDNA3.1-miR-942 into LH86 or HLCZ02 cells. [score:5]
All the data indicated that high expression of miR-942 might be one of the mechanisms acting to negatively regulate ISG12a in cancer cells. [score:4]
Overexpression of miR-942 or silencing ISG12a reversed TRAIL -induced apoptosis by AKT knockdown (Supplementary Fig. S6). [score:4]
Downregulation of ISG12a by miR-942 is needed to maintain the TRAIL-resistant phenotype of cancer cells and favors cancer cell survival, which might be the cell defense response to external harmful stimulation. [score:4]
Moreover, miR-942 is significantly upregulated in TRAIL-resistant Huh7 and HLCZ01 cells, verse TRAIL-sensitive LH86 and HLCZ02 cells (Fig. 4C). [score:4]
We postulate that AKT may regulate miR-942 expression. [score:4]
Here we demonstrate that miR-942 is upregulated in TRAIL-resistant cancer cells and decreased in TRAIL-sensitive ones. [score:4]
All the data suggested that the 3'UTR of ISG12a is a direct target of miR-942. [score:4]
MicroRNA-942 (miR-942) directly targets 3'UTR of ISG12a. [score:4]
AKT control TRAIL resistance of cancer cells through downregulation of ISG12a by miR-942. [score:4]
To elucidate the direct involvement of AKT on miR-942 expression levels, we analyzed the upstream sequence of miR-942 with the Promoter. [score:4]
Downregulation of ISG12a by miR-942 is needed to maintain the TRAIL-resistant phenotype. [score:4]
AKT controls TRAIL resistance of cancer cells through downregulation of ISG12a by miR-942. [score:4]
We predicted that ISG12a is a targeted gene of miR-942. [score:3]
MiR-942 is significantly upregulated in TRAIL-resistant cancer cells, verse sensitive cancer cells. [score:3]
The expression of miR-942 in the cells was detected by real-time PCR and normalized to U6. [score:3]
Interestingly, forced expression of miR-942 in LH86 or HLCZ02 cells significantly reduced the endogenous level of ISG12a (Fig. 6A) and changed the TRAIL sensitive phenotype to a resistant one, as the activation of PARP evidenced by appearance of cleaved PARP fragment was impaired (Fig. 6B). [score:3]
Forced expression of miR-942 in sensitive gastric cancer cell HGC-27 significantly reduced the endogenous level of ISG12a and changed the TRAIL sensitive phenotype to a resistant one (Supplementary Fig. S4A). [score:3]
Taken together, all the data indicate that the intracellular miR-942 may modulate sensitivity of cancer cells to TRAIL through targeting ISG12a with important implications in the design of new therapeutic agents. [score:3]
MiR-942 directly targets 3'UTR of ISG12a. [score:3]
Among the candidate targets, 3'UTR of human ISG12a contains region that matches the seed sequence of human miR-942 (Fig. 4B). [score:3]
Moreover, miR-942 is inversely correlated with ISG12a expression in 23 of 28 gastric cancer tissues (Fig. 5B). [score:3]
In the current study, the data indicated that miR-942 modulates TRAIL sensitivity in cancer cells mainly by targeting ISG12a. [score:3]
Conversely, when we performed luciferase assays using a plasmid harboring ISG12a3'UTR(Mut), where the binding sites for miR-942 were inactivated by site-directed mutagenesis, we did not observe inhibitory effect of miR-942 (Fig. 4B). [score:3]
All together, these data suggested that miR-942 modulates sensitivity of cancer cells to TRAIL -mediated apoptosis by targeting ISG12a. [score:3]
The reporter construct pGL3-ISG12aUTR and pcDNA3.1-miR-942 were used to transfect CHO cells, which express very low level of endogenous miR-942. [score:3]
The expression of TRAIL receptors is not affected by miR-942 (data not shown). [score:3]
Figure 6 (A) Forced expression of miR-942 in LH86 or HLCZ02 cells significantly reduced the endogenous level of ISG12a. [score:3]
The data further support the finding that ISG12a may be a target of miR-942 in vivo. [score:3]
To answer this question, we examined the expression of miR-942 and ISG12a by real-time PCR in primary liver cancer and gastric cancer tissue samples. [score:3]
However, it seems plausible that silencing of other targets of miR-942 contributes to TRAIL resistance in cancer cells. [score:3]
Of the 17 primary liver cancer tissues examined, miR-942 is inversely correlated with ISG12a expression in 15 liver cancer tissues (Fig. 5A). [score:3]
We found two DNA fragments containing the putative regulatory region upstream to miR-942(from +1~-600nt, +1~-2000nt). [score:2]
These results indicated that miR-942 promoting sequences are regulated by AKT. [score:2]
DNA fragments containing the putative regulatory regions upstream to miR-942 (from +1~-600 nt, +1~-2000 (+1 position corresponds to the 5' terminus of miR-942 hairpin) were amplified and cloned in pGL3basic (Promega). [score:2]
MiR-942 is inversely correlated with ISG12a expression in cancer tissues. [score:2]
Overexpression of miR-942 upon transfection markedly reduced the level of ISG12a compared to LH86 cells transfected with scrambled pre-miR (Fig. 4D). [score:2]
To further corroborate the negative regulation of miR-942 on TRAIL sensitivity in cancer cells, we delivered pcDNA3.1-miR-942 into HGC-27 cells. [score:2]
MiR-942 modulates the sensitivity of cancer cells to TRAIL -induced apoptosis by targeting ISG12a. [score:2]
pcDNA3.1-ISG12a were transfected into LH86 cells with or without pcDNA3.1-miR-942. [score:1]
2'-O-me-anti-miR-942 (5'-CACAUGGCCAAAACAGAGAAGA-3') & 2'-O-me-GFP miR (5'-AAGGCAAGCUGACCCUGAAGU-3') were from Takara. [score:1]
Increased expression of miR-942 upon transfection significantly decreased luciferase activity measured as relative luciferase activity (Fig. 4B). [score:1]
pGL3-ISG12a-UTR luciferase construct containing wild type or mutated (Mut) ISG12a 3'UTR was transfected into CHO cells together with pcDNA3.1-miR-942. [score:1]
In the figure the alignment of the seed region of miR-942 with 3'UTR of ISG12a is shown. [score:1]
The pearson correlation indicated that an inverse relation between miR-942 and ISG12a in cancer tissues exists. [score:1]
To validate this hypothesis, we cloned 3'UTR of ISG12a containing miR-942 binding sites into downstream of the luciferase open reading frame of pGL3 control vector. [score:1]
The pearson correlation indicated that an inverse relation between miR-942 and ISG12a in liver and gastric cancer tissues. [score:1]
LH86 cells were transfected with pcDNA3.1-miR-942, followed with TRAIL treatment for 4 hours. [score:1]
LH86 or HLCZ02 cells were transfected with pcDNA3.1-miR-942. [score:1]
Precursor of miR-942 was amplified from Huh7 cells and inserted into pcDNA3.1/V5-His. [score:1]
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2
[+] score: 107
The expression of miR-942 expression was downregulated in viral-infected cells at earlier phase and return to normal level at late phase. [score:8]
Moreover, silencing of ISG12a or overexpression of miR-942 decreased the expression of Noxa while it had no effect on Puma (Figure 7C). [score:5]
However, silencing of miR-942 expression by anti-miR-942 increased the expression of ISG12a in HLCZ01 cells and subsequently enhanced apoptosis triggered by HCV infection. [score:5]
The expression of ISG12a increased too fast to be inhibited by miR-942 at later phase. [score:5]
To examine whether miR-942 affects ISG12a expression in HLCZ01 cells, we examined the effect of forced expression of miR-942 on the level of ISG12a in HLCZ01 cells. [score:5]
MicroRNA-942 (miR-942) regulates HCV -induced apoptosis of human hepatocytes through targeting ISG12a. [score:4]
All the data supported that the ISG12a is a direct targeted gene of miR-942. [score:4]
The data suggested that miR-942 regulates HCV -induced apoptosis of human hepatocytes by targeting ISG12a. [score:4]
Moreover, miR-942 was markedly downregulated in HCV-infected HLCZ01 cells verse naïve HLCZ01 cells (Figure S3A). [score:4]
Expression of miR-942 was normalized with U6 (C). [score:3]
The expression of miR-942 was normalized with U6. [score:3]
To examined the effect of miR-942 on ISG12a expression and HCV -induced apoptosis of HLCZ01 cells, we transfected pcDNA3.1-miR-942 into HLCZ01 cells and detected the level of ISG12a and apoptosis of HLCZ01 in response to HCV infection. [score:3]
Overexpression of miR-942 upon transfection significantly decreased ISG12a level in comparison with the control (Figure S3E). [score:3]
All the data indicated that miR-942 modulates HCV -induced apoptosis of hepatocytes by targeting ISG12a. [score:3]
Forced expression of miR-942 in HLCZ01 cells markedly reduced ISG12a level and caused a marked decrease in HCV -induced apoptosis. [score:3]
MiR-942 regulated HCV -induced apoptosis of human hepatocytes through targeting ISG12a. [score:3]
The expression of miR-942 and ISG12a was examined by real-time PCR and normalized with U6 and GAPDH respectively. [score:3]
Forced expression of miR-942 in HLCZ01 cells markedly reduced ISG12a (Figure 6A and Figure S3E) and caused a strong decrease in apoptosis induction determined by flow cytometry (Figure 6B) and PARP cleavage (Figure 6C). [score:3]
Forced expression of miR-942 in HLCZ01 cells, confirmed by real-time PCR (Figure S3C), markedly reduced luciferase activity (Figure S3D). [score:3]
0094501.g006 Figure 6(A) Forced expression of miR-942 in HCV-infected HLCZ01 cells reduced the level of ISG12a. [score:3]
The expression of miR-942 or ISG12a was normalized with U6 or GAPDH respectively. [score:3]
So we proposed that ISG12a is a target of miR-942. [score:3]
Our data demonstrate that miR-942 was reduced in HCV-infected cells and ISG12a was a targeted gene of miR-942. [score:3]
MiR-942 modulates HCV -induced apoptosis of human hepatocytes through targeting ISG12a. [score:2]
When we performed luciferase assays using a plasmid harboring ISG12a3′UTR(Mut), where the binding sites for miR-942 were inactivated, we did not observe inhibitory effect of miR-942 on luciferase activity (Figure S3D). [score:2]
MiR-942 modulates HCV -induced apoptosis of human hepatocytes via targeting ISG12a. [score:2]
Knockdown of miR-942 by anti-miR-942 in HLCZ01 cells, which was confirmed by quantitative real-time PCR (Figure S3F), increased ISG12a protein level (Figure S3G). [score:2]
MiR-942 was inversely correlated with ISG12a expression in liver biopsies of chronic HCV-infected patients (Figure S3B). [score:2]
2′-O-me-anti-miR-942 (5′-CACAUGGCCAAAACAG AGAAGA-3′) and 2′-O-me-control-miR (5'-AAGGCAA GCUGACCCUGAAGU-3′) were from Takara. [score:1]
HCV-infected HLCZ01 cells were transfected with pcDNA3.1-miR-942. [score:1]
Precursor of miR-942 was amplified from Huh7 cells and inserted into pcDNA3.1/V5-His. [score:1]
HLCZ01 cells were transfected with pcDNA3.1-miR-942 and infected by HCV for 9 days. [score:1]
3′UTR of human ISG12a contains region that matches the seed sequence of human miR-942. [score:1]
HLCZ01 cells were transfected by pcDNA3.1-ISG12a shRNA or pcDNA3.1-miR-942, followed with HCV infection at MOI of 0.1 for 9 days. [score:1]
The reporter construct pGL3-ISG12aUTR and pcDNA3.1-miR-942 were transfected into HLCZ01 cells. [score:1]
Anti-miR-942 was delivered into HLCZ01 cells. [score:1]
Conversely, silencing miR-942 by anti-miR-942 in HLCZ01 cells increased ISG12a expression in HCV-infected cells (Figure 6D and Figure S3G) and enhanced apoptosis triggered by HCV infection measured by flow cytometry (Figure 6E) and PARP cleavage (Figure 6F). [score:1]
HLCZ01 cells were transfected with pcDNA3.1-miR-942 (pmiR-942). [score:1]
HLCZ01 cells were transfected by anti-miR-942 and infected by HCV for 9 days. [score:1]
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3
[+] score: 22
Hsa-miR-942 was an up-regulated, while hsa-miR-33a was a down-regulated miRNAs in ovarian cancer. [score:7]
The other four miRNAs, hsa-miR-942, hsa-miR-105, hsa-miR-150, and hsa-miR-27a* were identified to be up-regulated in ovarian cancer. [score:4]
There were 31 miRNAs interacted with hsa-miR-942 in MFSN, suggesting they were functionally synergistic with hsa-miR-942 and the expression changes of hsa-miR-942 in ovarian cancer may cause the changes of these connected miRNAs as well. [score:3]
The expression of miR-942 is significantly increased in patients with biliary tract cancer [22], and in late recurrent hepatocellular carcinoma samples [23]. [score:3]
The miRNA pairs comprised of hsa-miR-33a and hsa-miR-942 accounted for the richest functional module number of 279. [score:1]
GO: 0007268 (synaptic transmission) and GO: 0019226 (transmission of nerve impulse) were the two common functions of miRNAs in MFSN, and hsa-miR-579 (36), hsa-miR-942 (31), hsa-miR-105 (31), hsa-miR-150 (34), and hsa-miR-27a* (32) were selected as the hub nodes in MFSN. [score:1]
In all, 5 nodes with degrees more than 30, including hsa-miR-579 (36), hsa-miR-942 (31), hsa-miR-105 (31), hsa-miR-150 (34), and hsa-miR-27a* (32) were selected as the hub nodes in MFSN. [score:1]
The miRNA pair of hsa-miR-942 and hsa-miR-33a had the highest function module number of 279, and hsa-miR-942 as a hub node in MFSN, was synergistic with 31 miRNAs. [score:1]
According to their degrees in MFSN, hsa-miR-579, hsa-miR-942, hsa-miR-105, hsa-miR-150, and hsa-miR-27a* were selected as hub nodes in MFSN. [score:1]
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4
[+] score: 9
Other miRNAs from this paper: hsa-mir-26b, hsa-mir-128-2, hsa-mir-3190
Interacts with the tumor suppressor p53, and regulates p53 target gene expression hsa-mir-1273d chr1:10287776–10287861 Intron 1 Kinesin family member 1B (KIF1B) chr1:10,270,764–10,441,661 Transports mitochondria and synaptic vesicle precursors hsa-mir-3190 chr19:47,730,199–47,730,278 Intron 2 BCL2 Binding Component 3 (BBC3) chr19:47,724,079–47,736,023 Member of the BCL-2 family of proteins, cooperates with direct activator proteins to induce mitochondrial outer membrane permeabilization and apoptosis hsa-mir-942 chr1:117,637,265–117,637,350 Intron 18 Transcription Termination Factor, RNA polymerase II (TTF2) chr1:117,602,949–117,645,491 Member of the SWI2/SNF2 family of proteins Figure 4Different mechanisms of microRNA biogenesis. [score:9]
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5
[+] score: 8
MicroRNAs miR-190b, miR-630, miR-942, and miR-1284, the most frequent constituents of the classifiers generated in the current study, are not differentially expressed between cases and controls in the data-sets of either Keller, et al. or Leidinger, et al. as per the limma -based test used in the current study. [score:3]
Expression of miR-1284, miR-942, miR-630, and miR-190b. [score:3]
MicroRNAs miR-190b, miR-942 and miR-1284 were present in all of them. [score:1]
Overall, the two classification methods, SVM and TSP, identified four microRNAs (miR-190b, miR-630, miR-942, and miR-1284) that were present in a majority of the classifiers that were generated in the cross-validation analyses. [score:1]
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6
[+] score: 5
Of these, we highlighted 10 miRNAs (miR-9, miR-145*, miR-105, miR-147b, let-7f-2*, let-7i*, miR-302c*, miR-199a-3p, miR-222* and miR-942) whose expression was significantly higher at P<0.0005 (Fig. 3A ). [score:3]
Setting the specificity threshold to 100% showed the sensitivity level to be 88.9% for miR-9, miR-302c*, miR-199a-3p, and miR-222*; 77.8% in miR-145*, miR-105, and miR-942; and 66.7% in miR-147b, let-7f-2*, and let-7i*. [score:1]
The sensitivity level for miR-145*, miR-105, and miR-942 was 77.8%, and that for miR-147b, let-7f-2*, and let-7i* was 66.7% (Fig. 3B ). [score:1]
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7
[+] score: 3
Next, to further explore the functions of these miRNAs in HCC, we selected miRNAs with a fold change >5, namely hsa-miR-636, hsa-miR-671, hsa-miR-489, hsa-miR-26a, hsa-miR-320, hsa-miR-628, hsa-miR-505, hsa-miR-100, hsa-miR-664, hsa-miR-942, hsa-miR-192, hsa-miR-99b, hsa-miR-125b, hsa-miR-10b, hsa-miR-30b, and hsa-miR-145, for GO (Gene Ontology) enrichment analysis [21] of their target genes using the web -based software WebGestalt 2.0 [22]. [score:3]
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8
[+] score: 3
Also, Patnaik and colleagues identified microRNA expression profiles of whole blood in LAD, and showed that microRNAs miR-190b, miR-630, miR-942, and miR-1284 were the most frequent constituents of the classifiers [21]. [score:3]
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9
[+] score: 2
Diagnostic values were observed for let-7a-5p, let-7g-5p, miR-126-3p, miR-1248, miR-675, miR-942-5p, and miR-93-3p respectively in only two [9, 14], two [9, 10], one [9], two [10, 13], two [11, 13], two [12, 13], and four of the seven studies [9, 10, 12, 13]. [score:1]
The microRNAs that were examined were let-7a-5p, let-7g-5p, miR-93-3p, miR-126-3p, and miR-942-5p. [score:1]
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10
[+] score: 2
For the lung cancer patients five miRNAs (hsa-miR-3180-3p, hsa-miR-3200-5p, hsa-miR-4318, hsa-miR-942, hsa-miR-144*) were detected in all whole blood samples but not in any of the separated leukocyte subsets of lung cancer patients. [score:1]
In whole blood samples of healthy controls we found nine miRNAs (hsa-miR-130b*, hsa-miR-182, hsa-miR-183, hsa-miR-3180-3p, hsa-miR-3200-5p, hsa-miR-409-3p, hsa-miR-4318, hsa-miR-501-5p, hsa-miR-942) that were detected in all whole blood samples but not in any of the separated leukocyte subsets of healthy controls. [score:1]
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11
[+] score: 1
The second, a “C/T” SNP at chr1 62544469, was located in the 3’ strand of hsa-mir-942 and was present in one Hadza and two Sandawe individuals. [score:1]
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