〔Abstract〕 Objective To investigate the expression of miR-27a in colorectal cancer cell, and to analyze the effect of its targeted regulation of(Secreted Frizzled-Related Protein, SFRP1) on the biological behavior of colorectal cancer cells. Methods Real-time fluorescent quantitative PCR(qRT-PCR) was employed to examine the expression of miR-27a and SFRP1 mRNA in colorectal cancer tissues and adjacent normal tissues. Western blot was used to detect the expression of SFRP1 protein in colorectal cancer tissues and adjacent normal tissues. TargetScan software and dual luciferase reporter gene test were used to detect the targeted regulation of miR-27a on SFRP1.HCT116 cells were transfected with miR-27a mimic, miR-27a inhibitor and negtive control(NC). The expression of miR-27a and SFRP1 mRNA in each group was determined by qRT-PCR. MTT colorimetry was performed to evaluate the proliferation of each group cells. Transwell assay was used to evaluate the cell invasion and migration ability. Meanwhile, the protein expression levels of SFRP1, key factors Wnt4 and β-catenin in the Wnt/β-catenin signaling pathway were determined by Western blot. Results Compared with adjacent normal tissues, miR-27a was highly expressed in colorectal cancer tissues, while SFRP1 was low expressed in colorectal cancer tissues(P<0.05). TargetScan software and dual luciferase reporter gene test showed that miR-27a targeted SFRP1. Compared with NC group, the expression of miR-27a of miR-27a mimic group increased, the proliferation, invasion and migration ability enhanced, the expression of SFRP1 protein decreased, while Wnt4 and β-catenin protein expression increased(P<0.05). Compared with miR-27a mimic group, the expression of miR-27a of miR-27a inhibitor group decreased, the proliferation, invasion and migration ability reduced, the expression of SFRP1 protein increased, while Wnt4 and β-catenin protein expression decreased(P<0.05). Conclusion miR-27a can target SFRP1, inhibit the proliferation, invasion and migration of colorectal cancer cells, mainly by up-regulating SFRP1 and blocking the downstream Wnt/β-catenin signaling pathway, which provides a new direction for clinical treatment.