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The functional role of microRNA-23a (miR-23a) in tumorigenesis has been investigated;however,the exact mechanism of miR-23a in colorectal cancer development has not been fully explored.In the present study,we aimed to investigate the molecular functional role of miR-23a in colorectal carcinogenesis.Quantitative real-time polymerase chain reaction was conducted to investigate the expression level of miR-23a in tissue samples and cell lines (HCT116 and SW480).CCK-8,colony formation and Transwell assay were used to explore the role of miR-23a in cell proliferation and migration.Dual luciferase reporter assay was used to identify the direct binding of miR-23a with its target,MARK1.Weste blot analysis was used to analyze the expression level of MARK1,as well as a confirmed miR-23a target gene,MTSS1,in miR-23a-mimic and miR-23a-inhibit groups.Rescue experiments were conducted by overexpression of MARK1 in miR-23a-mimic-transfected cell lines.The results showed that miR-23a was highly expressed in colorectal cancer tissue and cell lines.MiR-23a could promote proliferation and migration of colorectal cancer cell lines.MARK1 was a direct target of miR-23a and the expression level of MARK1 was down-regulated in miR-23a-mimic-transfected cell lines but up-regulated in miR-23a-inhibit-transfected cells.Overexpression of MARK1 could partly reverse the cancer-promoting function of miR-23a.Our results suggested that miR-23a promotes colorectal cancer cell proliferation and migration by mediating the expression of MARK1.MiR-23a may be a potential therapeutic target for colorectal cancer treatment.