RESUMO
The present study aimed to investigate the function of microRNA25 (miR25) in human colon cancer cell viability and migration in addition to the underlying possible mechanisms. miR25 expression was upregulated in patients with colon cancer compared with the control group. Reverse transcriptionquantitative polymerase chain reaction and gene chip technology were used to analyze the alterations of miR25 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 ataxin3 (ATXN3), apoptosis regulator Bax (Bax) and cyclin D1. Overexpression of miR25 increased cell viability and migration, decreased apoptosis, decreased caspase3/9 activity level in addition to decreased Bax protein expression, and increased cyclin D1 protein expression in colon cancer cells. Furthermore, miR25 was demonstrated to target ATXN3 and suppress ATXN3 protein expression. Downregulation of miR25 induced apoptosis of colon cancer cells via increased expression ATXN3. Small interferingATXN3 inhibited the anticancer effects of miR25 downregulation in colon cancer. Collectively, the present results demonstrated that miR25 promoted human colon cancer cell viability and migration by regulating ATXN3 expression.