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目的:检测不同临床分期膀胱尿路上皮癌组织中微小RNA(miRNA，miR)-630的表达水平，探讨miR-630调控通路与膀胱尿路上皮癌临床病理特征之间的关系。方法:选用郑州大学第一附属医院2017年3月至2019年4月行手术切除并经病理证实的膀胱尿路上皮癌标本62例，每例标本均选用癌组织中心、癌旁组织及其远端正常黏膜对照。采用荧光定量反转录-聚合酶链反应(RT-PCR)和免疫组织化学技术检测切除标本中的miR-630、APC膜募集蛋白2(Amer2)和鸟嘌呤核苷酸交换因子(GEF-H1)的表达，并分析与各临床病理因素之间的关系。组间比较采用两独立样本n t检验。患者临床病理特征的分析采用n χ2检验。n 结果:miR-630在膀胱尿路上皮癌组织中的表达明显高于正常黏膜(0.913±0.215比0.624±0.195，n t＝2.133，n P<0.05)，差异有统计学意义，其在肌层浸润性尿路上皮癌中的表达高于非肌层浸润性(0.998±0.166比0.721±0.274，n t＝1.886，n P<0.05)，差异有统计学意义；Amer2在膀胱尿路上皮癌组织中的表达明显低于正常黏膜(0.828±0.235比1.683±0.612，n t＝-0.091，n P<0.05)，差异有统计学意义，与临床分期明显相关；Amer2下游调控因子GEF-H1在膀胱尿路上皮癌组织中的表达明显高于正常黏膜(1.712±0.192比1.125±0.554，n t＝-0.037，n P<0.05)，差异有统计学意义。相关分析显示miR-630与Amer2表达呈负相关(n r＝-0.537，n P<0.05)；Amer2与GEF-H1表达呈负相关(n r＝-0.613，n P<0.05)。n 结论:miR-630与膀胱尿路上皮癌临床分期及淋巴结转移明显相关，可能通过调控Amer2/GEF-H1通路，从而介导膀胱癌进展。“,”Objective:To detect the expression level of microRNA (miRNA, miR)-630 in the different clinical stages of bladder urothelial carcinoma (BUC), and explore the relationship between miR-630 pathway and clinicopathological features of BUC.Methods:A total of 62 cases of BUC specimens resected surgically were selected. For each specimen, the cancerous tissue and its remote normal mucosa were analyzed and compared. The expression of miR-630, Amer2 and GEF-H1 in resected cancer tissues was detected by Real-time RT-PCR, Western blotting and immunohistochemistry, and compared with clinicopathologic data. Two independent samples n t-test was used for comparison between groups. The clinicopathological features were analyzed by chi square test.n Results:The expression rate of miR-630 was significantly higher in BUC than in normal tissues (0.913±0.215 vs. 0.624±0.195, n t=2.133, n P<0.05), and that of miR-630 in non-muscle invasive bladder cancer group was significantly higher than that in non-muscle invasive group (0.998±0.166 vs. 0.721±0.274,n t=1.886, n P<0.05). The miR-630 was related with the degree of tumor differentiation and tumor depth of invasion. The expression of Amer2 in BUC tissues was significantly lowered in comparison with that in normal bladder epithelium (0.828±0.235 vs. 1.683±0.612,n t=-0.091, n P<0.05). GEF-H1, the downstream regulatory factors of Amer2, was significantly higher in BUC than in normal tissues (1.712±0.192 vs. 1.125±0.554,n t=-0.037, n P<0.05). Negative correlation was found between miR-630 and Amer2 (n r=-0.537, n P<0.05), and negative correlation was also found between Amer2 and GEF-H1 (n r=-0.613, n P<0.05).n Conclusion:The miR-630 was related with the clinical stages and lymph node metastasis of BUC through the regulation of Amer2/GEF-H1 pathway, which may mediate the occurrence and development of BUC.