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目的探讨miR-34c的表达及其基因启动子甲基化与肾癌的关系。方法采用实时定量-PCR检测41例肾癌组织及癌旁组织中miR-34c的表达,同时采用甲基化特异性PCR(MSP)方法检测miR-34c基因启动子甲基化情况。结果 miR-34c在肾癌组织的相对表达量低于癌旁组织(1.21±0.06vs.1.42±0.08)(P<0.05);miR-34c基因启动子甲基化在癌组织及癌旁组织的检测率差异无统计学意义(65.9%vs.51.2%)(P>0.05)。在31例Ⅰ期肾癌组织中,23例(74.2%)检测到miR-34c基因启动子的甲基化,明显多于癌旁组织的15例(48.4%)(P<0.05)。结论 miR-34c基因启动子甲基化是早期肾癌中miR-34c基因发生失活的原因之一,可能与肾癌的发生发展有关。
Objective To investigate the relationship between miR-34c expression and promoter methylation and renal cell carcinoma. Methods The expression of miR-34c in 41 cases of renal cell carcinoma and adjacent normal tissues was detected by real-time quantitative PCR. Methylation-specific PCR (MSP) was used to detect the promoter methylation of miR-34c gene. Results The relative expression level of miR-34c in renal cell carcinoma was lower than that in paracancerous tissues (1.21 ± 0.06 vs 1.42 ± 0.08, P <0.05). The methylation of miR-34c promoter in cancer tissues and paracancerous tissues The difference of detection rate was not statistically significant (65.9% vs.51.2%) (P> 0.05). Among 31 cases of stage I renal cell carcinoma, methylation of miR-34c promoter was detected in 23 cases (74.2%) than in adjacent non-cancerous tissues (48.4%) (P <0.05). Conclusion The promoter methylation of miR-34c gene is one of the causes of inactivation of miR-34c gene in early stage renal cell carcinoma, which may be related to the development of renal cell carcinoma.