Onco-miR-130 promotes cell proliferation and migration by targeting TGFßR2 in gastric cancer.

ABSTRACT

MicroRNAs (miRNAs) have been proved to play crucial roles in tumorigenesis. TGFß signal pathway abnormality is found in various cancers and correlates with tumor proliferation and metastasis. However, the mechanisms underlying the dys-regulation of TGFßR2 expression in GC have not been investigated yet. In this study, we found that the TGFßR2 protein was clearly repressed in tumor tissues, while miR-130 expression level was dramatically increased in GC tissues. Firefly luciferase activity assay revealed that miR-130 could directly bind to 3'UTR of TGFßR2 mRNA. Meanwhile, miR-130 mimics lead to the decreased TGFßR2 protein levels, while miR-130 inhibitors enhanced TGFßR2 expression in SGC7901 cells. Subsequent functional experiments showed that overexpressed miR-130 could promote proliferation and migration of SGC7901 cells. And siRNA-mediated TGFßR2 down-regulation could simulate the effects of miR-130 mimics on phenotypes of SGC7901 cells. Furthermore, there existed intense relationship between the expression level of miR-130 and epithelial-mesenchymal markers. Our results demonstrated that miR-130 was an oncogene by directly targeting TGFßR2 in GC.