Direct targeting of HGF by miR-16 regulates proliferation and migration in gastric cancer.

Related Articles

Direct targeting of HGF by miR-16 regulates proliferation and migration in gastric cancer.

Tumour Biol. 2016 Nov;37(11):15175-15183

Authors: Li S, Zhang H, Wang X, Qu Y, Duan J, Liu R, Deng T, Ning T, Zhang L, Bai M, Zhou L, Wang X, Ge S, Ying G, Ba Y

Abstract
MicroRNAs (miRNAs) have been reported to be involved in each stage of tumor development in various types of cancers. We have previously showed that miR-16 is downregulated in cancer and acts as a tumor suppressor. Other studies indicated that hepatocyte growth factor (HGF)/c-Met is implicated in proliferation, migration, and other pathophysiological processes. However, little is known about the relationship between miR-16 and HGF/c-Met in gastric cancer (GC). In the present study, we used bioinformatics tools and related experiments to search for miRNAs targeting HGF. Here, we found that miR-16 suppressed HGF protein expression by directly targeting 3'-untranslated region (UTR) of HGF mRNA. Subsequently, it was illustrated the downregulation of miR-16 promotes, while overexpressed of miR-16 significantly inhibits cell proliferation and migration by negatively regulating HGF/c-Met pathway. Moreover, the biological role of HGF in GC cells was determined by using HGF siRNA and HGF-overexpressing plasmid, respectively. To conclude, our results provide a potential target by using miR-16 for the future clinical treatment of GC.

PMID: 27683052 [PubMed - indexed for MEDLINE]

http://ift.tt/2djWkpT