Abstract
Colorectal cancer (CRC) is the most commonly diagnosed tumor worldwide. However, the molecular mechanisms and biological processes of CRC remain unknown. The present study used reverse transcription-quantitative polymerase chain reaction to determine the expression levels of microRNA (miR)-296 in CRC cell lines and tissues. In addition, a miR-296 mimic was transfected into CRC cells, and the effects of miR-296 on cell proliferation and apoptosis were explored by MTT assay and flow cytometry. Luciferase assays were also performed to validate arrestin β1 (ARRB1) as a miR-296 target in SW480 and HCT-116 cells. The results demonstrated that miR-296 is a critical tumor suppressor which was downregulated in CRC patients. Increased expression levels of miR-296 were positively associated with a longer survival time of CRC patients. In addition, it was demonstrated that ARRB1 is a direct downstream target of miR-296. Upregulation of miR-296 in SW480 and HCT-116 cells resulted in suppressed cell growth and increased cell apoptosis through an ARRB1-dependent mechanism. Furthermore, the molecular mechanisms underlying the antitumor effect of miR‑296 in CRC are at least in part due to the inactivation of the RAC-α serine/threonine-protein kinase (AKT) signaling pathway induced by the suppression of ARRB1 expression. Overall, the present study, to the best of the author's knowledge, is the first to demonstrate that the miR-296-ARRB1-AKT signaling pathway forms a critical feedback loop and mediates CRC carcinogenesis, and these findings may introduce a potential therapeutic strategy for the treatment of CRC.