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目的:探讨n miR-767-3p参与结直肠癌发病的确切机制。n 方法:收集临床原发性结直肠癌患者的结直肠癌组织及其相应癌旁正常组织标本60对，采用miRNA-RTPCR检测n miR-767-3p在人结直肠癌组织和细胞系中的表达水平。采用MTT、克隆形成检测n miR-767-3p对细胞增殖的影响。通过transwell实验分析确定其迁移和侵袭能力。采用双荧光素酶报告基因实验验证n miR-767-3p与其靶基因的直接相互作用。采用qRT-PCR检测细胞中的相关分子。通过n χ2检验及SPSS 17.0软件分析n miR-767-3p与结直肠癌患者临床病理特征之间的关系。n 结果:miR-767-3p在人结直肠癌组织中的表达明显低于癌旁组织，而且其在人结直肠癌细胞系中也是低表达。n miR-767-3p的表达与结直肠癌TNM分期(n χ2＝6.07，n P＝0.014)、肿瘤大小(n χ2＝7.59，n P＝0.006)及淋巴结转移(n χ2＝6.49，n P＝0.011)相关。在结直肠细胞系中(HCT116和SW480)过表达n miR-767-3p后，细胞的增殖、迁移和侵袭能力明显降低。n UGT2B17在人结直肠癌组织及细胞系中高表达。n miR-767-3p能够靶向调控n UGT2B17的表达。在结直肠细胞系中(HCT116和SW480)低表达n UGT2B17后，细胞的增殖、迁移和侵袭能力明显降低。在体内实验中，过表达n miR-767-3p能够抑制结直肠癌。n 结论:miR-767-3p的过度表达可通过下调结直肠癌中n UGT2B17的表达来抑制细胞增殖、迁移和侵袭，提示其可能是结肠癌患者的潜在治疗靶点。n “,”Objective:To explore the exact mechanism of n miR-767-3p in colorectal cancer.n Methods:Sixty pairs of colorectal cancer tissues and corresponding adjacent normal tissues from patients with primary colorectal cancer were collected. The expression of n miR-767-3p in human colorectal cancer tissues and cell lines was detected by miRNA RT-PCR. MTT and clone formation were used to detect the effect of n miR-767-3p on cell proliferation. The ability of migration and invasion was determined by transwell experiment. The direct interaction between n miR-767-3p and its target gene was verified by double luciferase reporter gene assay. qRT-PCR was applied to detect the related molecules in the cancer cell lines. The relationship between n miR-767-3p and clinicopathological characteristics of colorectal cancer patients was analyzed by chi-square test and SPSS 17.0 software.n Results:The expression of n miR-767-3p in human colorectal cancer tissues was significantly lower than that in adjacent normal tissues, and the expression of n miR-767-3p in human colorectal cancer cell lines was also low. The expression of n miR-767-3p was correlated with TNM stage (n χ2=6.07, n P=0.014), tumor size (n χ2=7.59, n P=0.006) and lymph node metastasis (n χ2=6.49, n P=0.011). Overexpression of n miR-767-3p in colorectal cell lines (HCT116 and SW480) could inhibit cell proliferation, migration and invasion. The low expression of n UGT2B17 in colorectal cell lines (HCT116 and SW480) significantly reduced the proliferation, migration and invasion of the cells. In vivo, overexpression of n miR-767-3p could inhibit colorectal cancer.n Conclusion:Overexpression of n miR-767-3p could inhibit the cell proliferation, migration and invasion by down-regulating the expression of n UGT2B17 in colorectal cancer, suggesting that n miR-767-3p may be a potential therapeutic target for colorectal cancer patients.n