A mi RNA s panel promotes the proliferation and invasion of colorectal cancer cells by targeting GABBR 1

Micro RNA s (mi RNA s) have been implicated in the regulation of colorectal cancer. Despite the expression of miR‐17‐92 cluster in cancer has been gradually revealed, the role of each individual mi RNA s in colorectal cancer still remains unclear. We studied the impact of miR‐106a/b, miR‐20a/b, and miR‐17 of miR‐17‐92 cluster on colorectal cancer cells. Real‐time quantitative polymerase chain reactions ( RT ‐ PCR ) were used to test these five mi RNA s expression in colorectal cancer cell line HCT 116. 3‐(4,5‐dimethyl‐2‐thiazolyl)‐2,5‐diphenyl‐2‐H‐tetrazolium bromide ( MTT ) assays, Bromodeoxyuridine (BrdU), and Transwell invasion assays were used to explore the effects of these five mi RNA s in colorectal cancer cells. Luciferase reporter assay, RT ‐ PCR , and western blotting were performed to validate the interaction of these five mi RNA s with the gamma‐amino‐butyric acid type B receptor 1( GABBR 1). We found that these five mi RNA s were significantly upregulated in colorectal cancer samples compared with normal tissues. Forced expression of these five mi RNA s significantly promoted HCT 116 and HT ‐29 cells proliferation and invasion. We further found that these five mi RNA s function as oncogenes in colorectal cancer by specifically binding to the 3‐untranslated regions (3′ UTR ) of GABBR 1.Furthermore, inhibition of GABBR 1 could mimic the function of mi RNA s in HCT 116 cells, while overexpression of GABBR 1 blocked the function of mi RNA s‐promoted proliferation and invasion. In conclusion, miR‐106a/b, miR‐20a/b, and miR‐17 contribute to the proliferation and invasion of colorectal cancer by targeting their common target gene, GABBR 1, and played a critical role in the proliferation and invasion of colorectal cancer.