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9 publications mentioning hsa-mir-1180

Open access articles that are associated with the species Homo sapiens and mention the gene name mir-1180. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 298
Other miRNAs from this paper: hsa-mir-21, hsa-mir-106a, hsa-mir-486-1, hsa-mir-486-2
Collectively, the results revealed that OTUD7B, TNIP2 and BAD are direct targets of miR-1180, and are subsequently downregulated in HCC cells overexpressing miR-1180. [score:9]
Moreover, we found that the direct targets of miR-1180 are OTUD7B, TNIP2 and BAD, and their expression is downregulated by the microRNA in HCC cells. [score:9]
We also examined the expression of the anti-apoptotic protein, Bcl-2, and the pro-apoptotic proteins, Bax and caspase-3. Overexpression of miR-1180 resulted in an increase of Bcl-2 expression, and a decrease of Bax and cleaved-caspase-3 expression (Fig. 2d, Supplementary Figure 2a). [score:9]
In summary, the present study demonstrates that the upregulation of miR-1180 contributes to the proliferation and cisplatin-resistance of HCC cells both in vitro and in vivo, by targeting and suppressing OTUD7B, TNIP2 and BAD. [score:8]
As predicted, western blotting revealed that the expression of OTUD7B, TNIP2 and BAD decreased in HepG2 and Huh7 cells overexpressing miR-1180, and expression increased in cells transfected with the miR-1180 inhibitor compared to negative controls (Fig. 5b). [score:8]
We also indicate a mechanism for miR-1180 induced drug resistance by downregulation of OTUD7B, TNIP2 and BAD, the direct targets of miR-1180 in HCC cells. [score:7]
Inhibition of miR-1180 attenuates cell viability and promotes cisplatin -induced apoptosis of HCC cells in vitroSuppression of miR-1180 (loss-of-function) studies using an inhibitor was performed to confirm the function of miR-1180 in HCC cells (Supplementary Figure 1b). [score:7]
Overexpression of miR-1180 enhanced the transcription of all target genes, whereas miR-1180 suppression clearly depressed gene transcription in HepG2 and Huh7 cell lines (Fig. 6c). [score:7]
Furthermore, inhibition of miR-1180 led to a decrease in Bcl-2 expression and an increase in Bax and cleaved-caspase-3 expression (Fig. 3d, Supplementary Figure 2b). [score:7]
Collectively, our results demonstrate that upregulation of miR-1180 activates NF-κB signaling via downregulation of OTUD7B and TNIP2, and thereby promotes the anti-apoptotic ability of HCC cells. [score:7]
In addition, we found that HCC patients with higher miR-1180 expression had a shorter survival time, whereas patients with lower miR-1180 expression had a longer survival time (n = 75; P = 0.001; Fig. 1d), suggesting a potential correlation between expression of miR-1180 and the progression of HCC. [score:7]
Inhibition of miR-1180 suppresses HCC cells proliferation and promotes cisplatin -induced apoptosis in vivoWe then examined the tumour suppressive role of a miR-1180 antagonist in HCC progression using an in vivo tumour mo del. [score:7]
miR-1180 modulates HCC cells survival through downregulation of its target genes, OTUD7B, TNIP2 and BAD. [score:6]
Ectopic overexpression of miR-1180 decreased the activity of OTUD7B-, TNIP2- or BAD-3′-UTR-luciferase reporters and miR-1180 suppression increased their activity (Fig. 5c–e). [score:5]
Moreover, the ratio of Bcl-2/Bax was significantly increased by miR-1180 overexpression and decreased by miR-1180 suppression, suggesting that miR-1180 increases the anti-apoptotic ability of HCC (Supplementary Figure 2c). [score:5]
However, when the OTUD7B-, TNIP2- or BAD-3′-UTR’s contained a mutated binding site (in the seed sequence), the luciferase activity was not affected by miR-1180 overexpression or suppression (Fig. 5c–e). [score:5]
Inhibition of miR-1180 with a miR-1180 antagonist (AntagomiR-1180) suppresses tumour growth and promotes cisplatin -induced apoptosis of HCC cells in vivo. [score:5]
As shown in Fig. 7a,b, and Supplementary Figure 5, miR-1180 expression in seven freshly collected HCC samples was inversely correlated with expression of OTUD7B (r = −0.673, P = 0.047) and TNIP2 (r = −0.709, P = 0.033); but was positively correlated with NF-κB activation (r = 0.761, P = 0.017). [score:5]
Suppression of miR-1180 (loss-of-function) studies using an inhibitor was performed to confirm the function of miR-1180 in HCC cells (Supplementary Figure 1b). [score:5]
Collectively, these results suggest that the inhibition of miR-1180 suppresses HCC cells proliferation and promotes cisplatin -induced apoptosis in vivo. [score:5]
The average miR-1180 expression was normalized using U6 expression. [score:5]
Moreover, the abundance of nuclear p65 significantly increased in the miR-1180 -overexpressing cells and was reduced when miR-1180 was suppressed (Fig. 6b, Supplementary Figure 3a). [score:5]
To explore the molecular mechanism of miR-1180 in HCC cells, the publicly available algorithms (TargetScan) were used to predict the target(s) of miR-1180 in humans. [score:5]
Moreover, Overexpression of OTUD7B or TNIP2 indeed antagonizes miR-1180 -induced NF-κB activation, which further confirmed our conclusion that miR-1180 -regulating OTUD7B (or TNIP2)- NF-κB- signaling regulation mediates HCC resistance (Fig. 6f and Supplementary Figure 4). [score:5]
Inhibition of miR-1180 suppresses cell viability and promotes cisplatin -induced apoptosis of HCC cells in vitro. [score:5]
Inhibition of miR-1180 suppresses HCC cells proliferation and promotes cisplatin -induced apoptosis in vivo. [score:5]
The expression levels of miR-1180 were normalized with reference to the expression levels of U6 small nuclear RNA (snRNA). [score:5]
To further confirm the direct correlation between miR-1180 and these putative target genes, the OTUD7B-, TNIP2- and BAD-3′-UTR fragments, containing the miR-1180 binding site, were subcloned into a pGL3 luciferase reporter vector. [score:4]
Importantly, intratumoural injection with an miR-1180 antagonist dramatically inhibited tumour growth, while injecting a antago-miR control had no effect on tumour development (Fig. 4a). [score:4]
To further explore the role of miR-1180 upregulation in HCC progression, we chose to examine the HepG2 and Huh7 cell lines (Supplementary Figure 1a). [score:4]
This increased activity of NF-κB signaling by miR-1180 is suggested to occur via downregulation of OTUD7B and TNIP2. [score:4]
In addition, our study shows that miR-1180 downregulates the BAD protein, which selectively binds to anti-apoptotic molecules of the Bcl-2 family to mediates its pro-apoptotic functions 42. [score:4]
As BAD is also downregulated by miR-1180, the mechanism may also contribute to cell survival in HCC. [score:4]
As OTUD7B and TNIP2 are common inhibitors of NF-κB signaling, we further examined this process and found that the NF-κB pathway was significantly activated by miR-1180, indicating its crucial role for apoptosis regulation might be through activation of NF-κB signaling in HCC cells. [score:4]
miR-1180 is upregulated in HCC. [score:4]
In the present study, we showed miR-1180 is upregulated in both HCC tissues and cell lines. [score:4]
Collectively, our results are consistent with the expected outcomes of an activated NF-κB signaling pathway, and provide evidence that miR-1180 contributes to cisplatin -induced resistance in HCC by targeting this pathway. [score:3]
We then examined the tumour suppressive role of a miR-1180 antagonist in HCC progression using an in vivo tumour mo del. [score:3]
On the other hand, miR-1180 suppression enhanced cisplatin -induced cell apoptosis. [score:3]
The results showed that OTUD7B, TNIP2 and BAD, which are closely correlated with cell survival and apoptosis progression in tumours, were three putative targets of miR-1180 (Fig. 5a). [score:3]
The expression of miR-1180, OTUD7B and TNIP2, and NF-κB activity in HCC tissues. [score:3]
Together, these results indicate that overexpression of miR-1180 in HepG2 and Huh7 cell lines can promote cell proliferation and provide resistance to cisplatin -induced cell death. [score:3]
MiR-1180 directly targets the 3′-UTR of OTUD7B, TNIP2, and BAD mRNA. [score:3]
We found miR-1180 was upregulated in eight samples of HCC tissues (T) compared with their adjacent noncancerous hepatic tissues (ANT; Fig. 1b). [score:3]
Ectopic overexpression of miR-1180 was capable of increasing the HCC cell growth and resistance to cisplatin -induced cell apoptosis both in vitro and in vivo. [score:3]
The miR-1180 mimic, miR-1180 inhibitor, negative control (NC), antagomiR-1180 and antagomiR control were purchased from RiboBio Co. [score:3]
These results strongly suggest that inhibition of miR-1180 attenuates cell viability and promotes cisplatin -induced apoptosis of HCC cells. [score:3]
As miR-1180 expression was elevated in HCC tissues and cell lines, miR-1180 appears to have a positive function on HCC progression. [score:3]
By analysing a published micro-array -based high-throughput assessment (NCBI/GEO/GSE36915), we found that miR-1180 was markedly upregulated in HCC tissues (T, n = 68), compared with that in non-tumour tissues (N, n = 21; P < 0.01; Fig. 1a). [score:3]
Finally, we examined whether miR-1180 -mediated OTUD7B and TNIP2 inhibition, and NF-κB signaling activation, in HCC cells was clinically relevant. [score:3]
To confirm the result of the published assessment, we examined the expression level of miR-1180 in our freshly collected HCC tissues using qRT-PCR. [score:3]
Cells were plated into a 6-well plate (1 × 10 [4] cells per well) and transfected with miR-1180 mimic, miR-1180 inhibitor, or NC. [score:3]
Ectopic miR-1180 promotes cell viability and inhibits cisplatin -induced apoptosis of HCC cells. [score:3]
Inhibition of miR-1180 attenuates cell viability and promotes cisplatin -induced apoptosis of HCC cells in vitro. [score:3]
Ectopic miR-1180 promotes proliferation and inhibits cisplatin -induced apoptosis of HCC cells. [score:3]
Clinical relevance of miR-1180 -mediated OTUD7B and TNIP2 inhibition and NF-κB activation in HCC. [score:3]
s showed that cells overexpressing miR-1180 showed fewer and smaller-sized colonies than control cells (Fig. 3b). [score:3]
MiR-1180 is upregulated in HCC. [score:3]
Inhibition of OTUD7B and TNIP2 results in activation of NF-κB, suggesting the anti-apoptotic function of miR-1180 may occur through the NF-κB signaling pathway. [score:3]
Similarly, in our study, we discover that miR-1180 is able to inhibit cisplatin -induced apoptosis of HCC cells. [score:3]
To further confirm miR-1180’s function on NF-κB signaling, cells transfected with miR-1180 were treated with an NF-κB inhibitor, JSH23, for 24 h. The MTS assay and colony formation assay both revealed that inhibition of NF-κB blocked the apoptosis resistant function of miR-1180 (Fig. 6d,e). [score:3]
Ectopic miR-1180 overexpression promoted NF-κB transcriptional activity compared to controls (Fig. 6a). [score:2]
Concurrently, apoptosis analysis using flow cytometry showed an increase in the percentage of Annexin-V-FITC -positive in cisplatin -treated and miR-1180 -inhibited HCC cells compared to the control cells (Fig. 3c). [score:2]
Flow cytometry experiments demonstrated that, after treatment with cisplatin (0.4 μg/ml, 24 h), the percentage of Annexin-V-FITC -positive HCC cells in cells that were overexpressing miR-1180 decreased significantly compared to the control cells (Fig. 2c). [score:2]
We first monitored the impact of ectopic overexpression of miR-1180 on cell viability using the MTS assay. [score:2]
The suppression of miR-1180 caused a significantly decreased cell viability compared to the control cells (P < 0.05; Fig. 3a). [score:2]
The expression of miR-1180 was also significantly increased (P < 0.05) across a panel of HCC cell lines (i. e., Hep3B, HepG2, BEL-7402, HCCC-9810, MHCC97H, MHCC97L, Huh7, and QGY-7703) compared to normal liver epithelial cells (THLE3; Fig. 1c). [score:2]
Activation of NF-κB signaling pathway is essential for the apoptosis resistant function of miR-1180 in HCC cells. [score:1]
In the present study, we observe that miR-1180 is also capable of augmenting the activity of NF-κB signaling to increase the apoptosis resistance of HCC cells. [score:1]
To further explore the function of miR-1180 on cytotoxic reagent -induced cell apoptosis, HCC cells were exposed to an anti-tumour agent, cisplatin. [score:1]
Our colony formation assays showed that overexpression of miR-1180 led to more and larger-sized colonies compared to control cells (P < 0.05; Fig. 2b). [score:1]
Meanwhile, the effect of miR-1180 on p50 nuclear translocation is the similar to that on p65 (Supplementary Figure 3b). [score:1]
A week later, mice in group A were injected intratumourally with 100 μl of a miR-1180 antagonist (diluted in PBS at 2 mg/ml), and mice in group B were injected with a antagomiR control (diluted in PBS at 2 mg/ml), three times per week. [score:1]
These experiments indicate that miR-1180 promotes the resistance to cisplatin-induce apoptosis in HCC cells through activation of the NF-κB signaling pathway. [score:1]
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2
[+] score: 12
The expression levels of miR-17-5p, miR-593, miR-23a-5p, miR-586, miR-1180, miR-508-5p, miR-511, miR-646, miR-634, miR-149-5p, miR-24-3p, miR-1267, miR-504 and miR-1270 were upregulated (Fig. 2A) (P<0.05). [score:6]
The expression levels of miR-17-5p, miR-593, miR-23a-5p, miR-586, miR-1180, miR-508-5p, miR-511, miR-646, miR-634, miR-149-5p, miR-24-3p, miR-1267, miR-504 and miR-1270 were upregulated. [score:6]
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3
[+] score: 5
Other miRNAs from this paper: hsa-mir-370, hsa-mir-373, mmu-mir-370, hsa-mir-1236
And we also proved that miR-1236, miR-1180 and miR-370 could activate the expression of suppressor gene p21 [34– 36]. [score:5]
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4
[+] score: 4
Using, miR-887, miR-1306, miR-1180, miR-1268, miR-371-5p, miR-630, and miR-595 exhibited enrichment of seed regions in the set of mRNAs down-regulated 20 hours after IR. [score:4]
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5
[+] score: 4
Locus ID Gene RefSeq Expression Phastcons Status 21019 Intron - AC124066.2 1,12,2,1 0.57 miR-1180 38843 Intron ARL10 - 0,0,3,2 0.99 miR-1271 6150 Intron C10orf33 - 4,0,1,4 1 miR-1287 6746 Intron JMJD1C - 1,4,2,1 1 miR-1296 27738 Intron DNMT3A - 3,12,7,4 0.99 miR-1301 8884 intron FADS1 NM_013402 2,0,9,2 0.34 miR-1908 37600 repeat - - 136,933,146,220 0.03 alt. [score:3]
While writing this paper a new version of miRBase was released, now including six of these miRNAs (mir-1180, mir-1271, mir-1287, mir-1296, mir-1301, and mir-1908). [score:1]
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6
[+] score: 3
14 miRNAs were mutually deregulated (mir-1180, -125b, -135b*, -138, -19a, -221, -31, -31*, -372, -375, -378, -455-3p, -517c, -522), of which four were mutually deregulated by over 2-fold each (miR-135b*, -138, -375, -522). [score:3]
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7
[+] score: 2
MiR-1308 and miR-1180 were also deregulated by greater than 2-fold in tamoxifen treated MCF-7/HER2Δ16 cells. [score:2]
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8
[+] score: 1
MRESS SNPs FST Gene miR CNM SNPs FST Gene miR rs3822506 0.8743 TCERG1 miR-590 rs7665492 0.8942 ENAM miR-3916 rs1217382 0.8469 BCL2L15 miR-17 rs1043809 0.8900 EPN2 miR-3616-3p rs3087542 0.8428 EMCN miR-197 rs2470102 0.8859 MYEF2 miR-1180 rs3742988 0.8385 CDAN1 miR-378 rs7290134 0.8695 TNFRSF13C miR-1205 rs1071738 0.8298 PALLD miR-182 rs8057598 0.8596 NOL3 miR-769-3p rs1969589 0.8545 RGMA miR-593* rs1246014 0.8476 COPS7B miR-1273d rs12449157 0.8399 GFOD2 miR-125a-3p rs16990309 0.8398 SLC23A2 miR-760 rs3742988 0.8385 CDAN1 miR-326 rs2292549 0.8361 GPBAR1 miR-936 rs1995939 0.8338 STARD9 miR-3943 rs3199486 0.8321 STARD9 miR-2278 rs873258 0.8312 TSPAN14 miR-873MRESS and CNM SNPs showing highest levels of population sub-division among HapMap phase 3 data- All SNPs falling 2 SDs from the mean F [ST ]of 3'UTR SNPs. [score:1]
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9
[+] score: 1
Furthermore, miRNA profiles of peripheral blood mononuclear cells isolated from Brazilian GDM women, obtained by using microarray platforms, have identified ten miRNA that seemed to be specific for GDM, namely, miR-101, miR-1180, miR-1268, miR-181a, miR-181d, miR-26a, miR-29a, miR-29c, miR-30b and miR-595 [(] [67] [)]. [score:1]
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