MicroRNA-613 targets FMNL2 and suppresses progression of colorectal cancer

Increasing evidence indicates that dysregulation of miRNAs is involved in the initiation and progression of colorectal cancer (CRC). MicroRNA (miR)-613 has been reported to function as a tumor suppressor in many cancers. However, the precise role of miR-613 in CRC progression is unclear. This study aimed to investigate the role and underlying mechanism of miR-613 in growth and metastasis of CRC. Real-time quantitative PCR (qPCR) and western blot techniques were used to assess expression of miR-613 and formin-like 2 (FMNL2) in CRC cell lines and tissues. Luciferase reporter assays were conducted to investigate the association between miR-613 and FMNL2. Proliferation, wound healing, and transwell invasion assays, as well as flow cytometric analysis, were performed to evaluate the effect of miR-613 on proliferation, migration, invasion, and cell-cycle status, respectively, of CRC cells. We found that miR-613 was significantly downregulated in CRC cell lines and tissue samples, and correlated closely with TNM stage. miR-613 suppressed CRC cell proliferation, migration, and invasion, and induced cell-cycle arrest at G1 phase. FMNL2 was identified as a direct target of miR-613 in CRC cells. Importantly, FMNL2 overexpression rescued miR-613-induced suppression of proliferation, migration, and invasion of CRC cells. These results suggest that miR-613 functions as a tumor suppressor in the progression of CRC by regulating FMNL2.