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目的 探讨转录因子激活蛋白2E(transcription factor activator protein 2E,TFAP2E)在胃癌细胞株的甲基化水平及其对5-氟尿嘧啶(5-fluorouracil,5-Fu)敏感性的影响.方法 采用不同浓度5-氮杂-2-脱氧胞苷(5-Aza-2-deoxycytidine,5-Aza-CdR)去甲基化处理2种胃癌细胞株BGC823、SGC7901,运用甲基化敏感性高分辨率熔解曲线(methylation-sensitive high-resolution melting,MS-HRM)技术检测TFAP2E基因甲基化状态;Western blot检测TFAP2E蛋白表达情况.采用不同浓度的5-Fu作用于去甲基化处理的细胞株,用CCK8法检测细胞存活率.结果 (1)2种胃癌细胞株经5-Aza-CdR去甲基化处理后,TFAP2E甲基化水平下降,TFAP2E蛋白表达水平显著提高(P<0.05),呈浓度依赖性;(2)经5-Aza-CdR去甲基化处理后,2种胃癌细胞株对5-Fu的敏感性明显增强(P<0.01),呈剂量依赖性.结论 TFAP2E甲基化水平越高,胃癌细胞对5-Fu的敏感性越低.“,”Objective To explore the relationship between the transcription factor activator protein 2E (TFAP2E) methylation level and 5-fluorouracil (5-Fu) sensitivity in human gastric cancer cell lines. Methods Two kinds of human gastric cancer cell lines (BGC823, SGC7901) were treated with 5-Aza-2-deoxycytidine (5-Aza-CdR) at different concentrations. The methylation status of TFAP2E was examined by methylation-sensitive high-resolution melting (MS-HRM). The protein expression levels were detected by Western-blot analysis. Gastric cancer cell lines with 5-Aza-CdR intervened were treated with distinct concentrations of 5-Fu, and cell viability was observed by CCK8 assay. Results (1)5-Aza-CdR reduced the methylation level of TFAP2E and significantly increased TFAP2E protein expression (P<0.05) in BGC823 and SGC7901 in a dose-dependent manner; (2) After the treatment of 5-Aza-CdR, 5-Fu resulted in a significant decrease in cell viability in both of the two cell lines (P<0.01), also in a dose-dependent manner. Conclusion TFAP2E hypermethylation was associated with nonresponse to 5-Fu exposure in vitro study.