摘要目的 观察结直肠癌与毗邻癌旁组织中microRNA-221(miR-221)与细胞周期蛋白依赖性激酶抑制因子p57(CDKN1C/p57)的差异表达.方法 常规抽提结直肠癌及对照癌旁组织中总RNA及蛋白质,应用实时荧光定量聚合酶链反应(PCR)检测标本中miR-221表达,以半定量逆转录(RT)-PCR和Western blot分析CDKN1C/p57 mRNA和蛋白表达.结果 30例结直肠癌与癌旁组织相比,miR-221表达明显上调(2.041±1.401比0.806±0.341),差异有统计学意义(P＜0.01),半定量RT-PCR和Western blot分别证实其可能调节的靶目标CDKN1C/p57在mRNA水平结直肠癌和癌旁组织中表达差异无统计学意义(P＞0.05),而蛋白质水平在结直肠癌中表达明显下降(3.019±1.708比0.972±0.316,P＜0.01).结论 miR-221可能通过转录后基因沉默机制使CDKN1C/p57蛋白表达下降,从而促进结直肠癌的发生发展.

abstractsObjective To investigate the differential expression of microRNA-221 (miR-221) and CDKN1C/p57 in colorectal carcinoma and adjacent non-tumorous tissues. Methods The colorectal carcinoma and adjacent non-tumorous tissues were collected respectively and the total RNA and protein were isolated routinely. The miR-221 expression pattern was detected by real-time quantitative polymerase chain reaction (PCR) following the protocols recommended by the commercial corporation. CDKN1C/p57 mRNA and corresponding protein expression patterns were detected by semi-quantitative reverse transcription(RT)-PCR and Western blotting. Results The expression of miR-221 was significantly up-regulated in colorectal carcinoma tissues as compared with that in the adjacent non-tumorous tissues (2. 041 ± 1. 401 vs 0.806 ±0.341 ,P ＜0.01 ). RT-PCR and Western blotting analysis demonstrated that there was no significant difference in CDKN1C/p57 (the possible target of up-regulated miR-221 ) mRNA expression between colorectal carcinoma and non-tumorous tissues, whereas CDKN1C/pS7 protein was markedly decreased in colorectal carcinoma ( 3.019 ± 1. 708 vs 0. 972 ± 0. 316, P ＜ 0. 01 ). Conclusion MiR-221 could inhibit CDKN1C/p57 expression by post-transcriptional gene silencing to promote colorectal carcinoma occurrence and progress.