Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Pseudogene INTS6P1 regulates its cognate gene INTS6 through competitive binding of miR-17-5p in hepatocellular carcinoma [miRNA]

ABSTRACT: To identify the novel tumor suppressors in hepatocellular carcinoma (HCC), we have employed whole genome microarray expression profiling as a discovery platform in HCC and paired normal liver tissues to identify genes which down-regulated in HCC. Among which, INTS6 and its pseudogene, namely INTS6P1, were found to be dramatically down-regulated in HCC. The down-regulated expression of INTS6 and INTS6P1 in HCC was further confirmed by real-time PCR. RNA was extracted from 3 pairs of HCC and normal liver tissue harvested from patients to undergo microarray study.

ORGANISM(S): Homo sapiens

SUBMITTER: Florin Selaru

PROVIDER: E-GEOD-64632 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:From the results of microarray, 7616 miRNAs with significantly different expression ratios were selected when CNE-2-S-18/SP cells were treated with DC120. Among these, 80 miRNAs were up-regulated and 78 were down-regulated. We then chose 20 miRNAs through the qRT M-bM-^@M-^S PCR, and our results showed that 9 miRNAs were up-regulated after treatment with DC120, which was consistent with the results of the microarray. Among these, miR-30a were significantly up-regulated. These results indicated that miR 30a expression was up-regulated by DC120. We then investigated the role of miR 30a in DC120-treated cells, we explored its potential targets using a bioinformatics approach of complementary base pairing. The relative luciferase activity of the reporter that contained the wild type 3' UTR was significantly suppressed when miR 30a was contransfected. In contrast, the luciferase activity of the mutant reporter was unaffected by the contransfection of miR 30a, indicating that miR 30a suppressed Sox2 gene expression using the miR 30a binding sequence at the 3' UTR of the Sox2 gene. Additionally, the ectopic expression of miR 30a caused a decrease in Sox2 protein expression and mRNA levels in CNE-2-S-18 cells. These data demonstrate that miR 30a may directly target the Sox2 gene via seed matches on both 3' UTR. Taken together, our results demonstrate that DC120 regulates Sox2 via up-regulation of miR 30a. In this study, two samples were used to acquire the miRNA expression profiling. We analyzed the differences in miRNA profiles between control (DMSO solution) and DC120 treatment in CNE-2-S-18/SP cells from miRNA microarrays. The CNE-2-S-18/SP cells were separately cultured with a DMSO solution or 10M-NM-<mol/L DC120 for 15h, and total RNA from all of the cells was extracted. Then we chose 20 up-regulated miRNAs through the qRT M-bM-^@M-^S PCR, and our results showed that 9 miRNAs were up-regulated after treatment with DC120. Among these, miR-30a were significantly up-regulated. Then we investigated the role of miR 30a in DC120-treated cells by bioinformatic methods and Dual luciferase reporter system, the function of miR-30a was analyzed through ectopic expression of miR 30a. Taken together, our results demonstrate that DC120 regulates Sox2 via up-regulation of miR 30a.

Dataset Information

Pseudogene INTS6P1 regulates its cognate gene INTS6 through competitive binding of miR-17-5p in hepatocellular carcinoma [miRNA]

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