Objective To investigate the role of miR-3917 in the proliferation and migration of colorectal cancer(CRC)cells and associated signaling pathway mechanism.Methods GEO2R tool was used to analyze the miRNA ex-pression dataset(GSE101502)to obtain differentially expressed miRNAs in CRC tissues.The expression level of target miRNA was verified in the sample expression data from TCGA database.The expression levels of miR-3917 in human normal colon cell line(CCD841 CoN)and CRC cell line(HCT 116)were detected by qPCR.The expression of miR-3917 was up-regulated by transfecting its mimic in HCT 116 cells,and the expression was verified by qPCR.The cell prolif-eration was assessed by CCK-8 assay and plate colony formation assay.The cell migration was assessed by wound-heal-ing assay and Transwell migration assay.The target genes of miR-3917 were predicted using TargetScan,and enrich-ment analysis was performed with DAVID database.The expression of nuclear β-catenin protein was detected by West-ern blot to evaluate the activation level of Wnt/β-catenin signaling pathway.Results A total of 21 differentially ex-pressed miRNAs(Log2 | Fold Change |>1,P<0.05)were identified,of which 2 were up-regulated and 19 were down-regulated in CRC tissues compared to normal tissues.The expression of miR-3917 significantly decreased in CRC tissues(P<0.05).Compared with the CCD841 CoN cell line,the expression of miR-3917 in HCT 116 cell line signifi-cantly decreased(P<0.05).Transfecting miR-mimic in HCT 116 cells could significantly up-regulate the expression of miR-3917(P<0.05).The proliferation(CCK-8 assay,P<0.05;plate colony formation assay,P<0.05)and migration(wound-healing assay,P<0.05;Transwell assay,P<0.05)abilities of HCT 116 cells in the miR-mimic group signifi-cantly decreased compared with those in the control group.The Wnt/β-catenin signaling pathway of HCT 116 cells in the miR-mimic group was significantly inhibited(P<0.05)compared with that in the control group.Conclusion miR-3917 inhibits the proliferation and migration of CRC cells by regulating the Wnt/β-catenin signaling pathway,which provides a potential new target for the treatment of CRC.