Full-text resources of PSJD and other databases are now available in the new Library of Science.
Visit https://bibliotekanauki.pl
Preferences help
enabled [disable] Abstract
Number of results

Results found: 1

Number of results on page
first rewind previous Page / 1 next fast forward last

Search results

help Sort By:

help Limit search:
first rewind previous Page / 1 next fast forward last
|
2015
|
vol. 62
|
issue 1
77-82
EN
Dysregulation of miRNA is widely involved in human cancers, including hepatocellular carcinoma (HCC). Array data for miRNAs indicated that miR-331-3p might be one of the disorderly expressed miRNAs in HCC cell lines, but the function of miR-331-3p in HCC remains unclear. In this study, quantitative real time polymerase chain reaction (qRT-PCR) results indicated that miR-331-3p was up-regulated in HepG2.2.15 cells, Ad-HBV-HepG2 cells and pCH9/3091transfected SMMC7721 cells compared with their control group, respectively. miRNA target prediction software was used, and VHL was found to be one of the target genes of miR-331-3p. qRT-PCR and western blot analysis indicated VHL expression was decreased when miR-331-3p was over-expressed and increased when miR-331-3p was inhibited in SMMC7721 cells. The luciferase reporter activity was inhibited in SMMC7721 cells when co-transfected with miR-331-3p expression vector and VHL 3'-UTR wild type vector and increased in HepG2.2.15 transfected with miR-331-3p inhibitor compared to its control group respectively. When co-transfected with miR-331-3p expression vector and VHL 3'-UTR mutated type vector in SMMC7721 cells the luciferase reporter activity was recovered. All of these results show that HBV up-regulated miR-331-3p expression in HCC cell lines and miR-331-3p could inhibit VHL expression by directly targeting its 3'-UTR. This provided useful information in exploring the mechanism of HCC induced by HBV infection.
first rewind previous Page / 1 next fast forward last
JavaScript is turned off in your web browser. Turn it on to take full advantage of this site, then refresh the page.