目的检测CDH11基因启动子在肾癌中的甲基化情况,并分析甲基化与临床病理特征的关系。方法通过甲基化特异性PCR(MSP)检测CDH11基因在5株肾细胞癌细胞系、1株正常肾细胞系、46例肾细胞癌组织、23例癌旁肾组织,以及10例非肾实质肿瘤正常。肾组织中的甲基化状态。将甲基化情况与患者I临床资料联系,进行统计学分析。结果CDH11在5株肾癌细胞系中,有3株出现甲基化,甲基化率为60%;在人正常肾细胞系中未检测到甲基化。CDH11在肾癌组织中的甲基化率为45.7%(21/46),显著高于癌旁肾组织(26.1%,6/23)及非肾实质肿瘤正常肾组织(0,(3/10),差异具有统计学意义(P〈0.05)。肾细胞癌各分期间及各分级间,癌组织中CDH11基因甲基化检出率无统计学意义(P〉0.05);左侧肾癌与右侧肾癌相比,癌组织CDH11基因甲基化率差异无统计学意义(P〉0.05);男性肾癌患者与女性肾癌患者相比,肾癌组织中CDH1基因甲基化率差异无统计学意义(P〉0.05)。结论肾细胞癌组织中CDH11基因甲基化率显著高于癌旁正常肾组织及非肾实质肿瘤正常肾组织,且癌组织中CDH11基因甲基化率与临床病理资料如肿瘤分期及分级无显著相关性,提示CDH11基因甲基化是。肾细胞癌发生中的早期频发事件,可能是。肾细胞癌独特的基因甲基化谱成员之一,并在肾细胞癌的早期诊断上发挥作用。
Objective To investigate the promoter methylation status of Cadherin-11(CDH11) and its relation with clinicopathological features in renal cell carcinoma(RCC), which further clarifies the effects of CDH11 on RCC tumorigenesis and identifies a new epigenetics biomarker for early diagnosis of RCC. Methods CDH11 methylation was detected by methylation specific PCR(MSP) in five RCC cell lines and 46 cases of RCC primary tumors. We selected one normal renal cell line, 23 cases of adjacent non-tumor renal tissues and 10 cases of normal kidney tissues from renal pelvic carcinoma as controls. Patients' clinicopathological features were collected and analyzed. Results MSP revealed that CDH11 gene promoter was methylated in 3 of 5 RCC cell lines, and in 45.7% of renal primary tumors patients. 6 of 24 (26.1%) adjacent normal renal tissues showed methylation. No methylation was detected in normal renal cell line and normal kidney tissues from renal pelvic carcinoma. The methylation of CDH11 was not associated with gender, location, tumor nuclear grade and TNM classification. Condusions The CDH11 promoter methylation rates in RCC were significantly higher than those in normal controls(46.25% vs. 23%, 46.25% vs. 0%, both P〈0.05). Our results indicated that CDH11 gene methylation as a frequently early event involve in RCC tumorigenesis may be used as an effective index to diagnose RCC.