MicroRNA-195 suppresses colorectal cancer cells proliferation via targeting FGF2 and regulating Wnt/β-catenin pathway

Colorectal cancer (CRC) is a prevalent cancer with high mortality worldwide. This study was aimed to explore the functional effects of microRNA-195 (miR-195) on CRC cells and the underling mechanism involved. quantitative PCR (qPCR) was performed to monitor the expression of miR-195 in CRC tissues and cell lines. SW480 and SW620 cells were transfected with either miR-195 mimic or antisense oligonucleotides (ASO) of miR-195. Then cell viability, cell cycle and the expressions of CyclinB1, CyclinD1 and Cyclin-Dependent Kinase 2 (CDK2) were respectively detected by 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyltetrazolium bromide (MTT), flow cytometry, qPCR and Western blot. A target of miR-195 was predicted and verified in vitro by using TargetScan and microRNA database, Dual-Luciferase reporter assay, qPCR and Western blot. Further, the functions of the target on cell viability and cell cycle were detected by transfection with its expression vector. Moreover, the expressions of Wnt/beta-catenin pathway proteins were detected by qPCR and Western blot. Results show that MiR-195 was decreased during CRC, and miR-195 overexpression inhibited cell viability, arrested cells in G2/M phase, and down-regulated CyclinB1, CyclinD1 and CDK2 (P < 0.05 or P < 0.01). Fibroblast growth factor 2 (FGF2) was a direct target of miR-195 and alleviated the inhibitive effects of miR-195 on cell viability and cell cycle progression (P < 0.05 or P < 0.01). Further, miR-195 specifically regulated Wnt/beta-catenin pathway proteins (P < 0.01). All these findings suggest that miR-195 suppressed CRC cells proliferation via targeting FGF2 and blocking Wnt/beta-catenin pathway.