雄激素受体基因甲基化与食管癌的分级

 目的研究食管癌组织中雄性激素受体(AR)基因的5’端CpG岛的甲基化状态及其与食管癌分级的关系,探讨其与肿瘤生物学特性的相关性。方法应用限制性内切酶(HpaII,MspI和HhaI)和PCR扩增方法,对48例食管癌组织和34例癌旁组织AR的5’端CpG岛的甲基化状态分析,并进行不同级别间的比较及统计学分析。结果48例食管癌组织中HhaI位点甲基化占45.8%,HpaII位点甲基化占56.3%;34例癌旁组织中HhaI位点甲基化占61.8%,HpaII位点甲基化占58.8%,男性不同级别癌组织的甲基化程度均比癌旁组织低,随着级别的上升癌及癌旁组织甲基化程度也随着上升;对28例同一个体的癌及癌旁组织研究发现发生甲基化改变的占39.3%,其中程度降低占72.7%,均为男性。结论雄性激素受体基因去甲基化可能是食管癌发生发展的重要始动因素之一,为进一步研究采用抗雄性激素防治食管癌提供了实验依据。

Methylation of Androgen-receptor Gene and the Grade of Esophageal Cancer

Objective To observe the methylation of the first exon of the Androgen receptor gene, and its possible association with esophageal cancer. Methods The methylation of the first exon of the Androgen receptor gene was studied by PCR using restriction enzymes Hpa II , Msp I and HhaI in 48 esophageal cancer Tissues(squamous cell carcinomas) and 34 pericancerous non tumor tissues in Shanxi people.Results The methylation rates of HhaI and HpaII sites of the Androgen receptor gene in esophageal cancer tissues and pericancerous non tumor tissues were 45.8% , 56.3% ; 61.5% , 58.8% . The methylation rates of HpaII and HhaI sites of the Androgen receptor gene in different grades of male esophageal cancer tissues were lower than those of pericancerous non tumor tissues. The methylation rates of HpaII and HhaI sites in high differentiated was less obvious than that in low and moderate differentiated esophageal cancer tissues and pericancerous non tumor tissues. The change of methylation status of the androgen receptor gene were found in 11 cases. The methylation of the androgen receptor gene were decreased in 8 cases.Conclusion These findings suggest a potential role of hepomethylation of androgen receptor gene in esophageal cancer. That is an impetus for further studies to assess anti androgen therapy for treatment and or prevention of esophageal cancer.