MicroRNA-25/ATXN3 interaction regulates human colon cancer cell growth and migration

The present study aimed to investigate the function of microRNA-25 (miR-25) in human colon cancer cell viability and migration in addition to the underlying possible mechanisms. miR-25 expression was upregulated in patients with colon cancer compared with the control group. Reverse transcription-quantitative polymerase chain reaction and gene chip technology were used to analyze the alterations of miR-25 in patients with colon cancer. Cell viability and cell migration were analyzed using MTT and wound healing assays, respectively, apoptosis was analyzed using flow cytometry, and western blot analysis was conducted to determine the protein expression of ataxin-3 (ATXN3), apoptosis regulator Bax (Bax) and cyclin D1. Overexpression of miR-25 increased cell viability and migration, decreased apoptosis, decreased caspase-3/9 activity level in addition to decreased Bax protein expression, and increased cyclin D1 protein expression in colon cancer cells. Furthermore, miR-25 was demonstrated to target ATXN3 and suppress ATXN3 protein expression. Downregulation of miR-25 induced apoptosis of colon cancer cells via increased expression ATXN3. Small interfering-ATXN3 inhibited the anti-cancer effects of miR-25 downregulation in colon cancer. Collectively, the present results demonstrated that miR-25 promoted human colon cancer cell viability and migration by regulating ATXN3 expression.