上海交通大学学报（医学版）

›› 2011, Vol. 31 ›› Issue (1): 95-.doi: 10.3969/j.issn.1674-8115.2011.01.022

• 综述 • 上一篇    下一篇

DNA修复相关基因启动子甲基化和肿瘤化疗耐药的进展

韩 婧, 李 江   

  1. 上海交通大学 医学院附属第九人民医院口腔病理科 上海市口腔医学重点实验室, 上海 200011
  • 出版日期:2011-01-28 发布日期:2011-02-01
  • 通讯作者: 李 江, 电子信箱: lijiang182000@yahoo.com。
  • 作者简介:韩 婧（1985—）, 女, 硕士生；电子信箱: hanjing2008@sjtu.edu.cn。
  • 基金资助:

    国家自然科学基金（30872905，81072211）；上海市重点学科建设项目（S30206）；上海市科委基金（08DZ2271100）

Research progress of promoter methylation of DNA repair related genes and tumor chemoresistance

HAN Jing, LI Jiang   

  1. Department of Oral Pathology, The Ninth People's Hospital, Shanghai Jiaotong University School of Medicine, Shanghai Key Laboratory of Stomatology, Shanghai 200011, China
  • Online:2011-01-28 Published:2011-02-01
  • Supported by:

    National Natural Science Foundation of China, 30872905, 81072211；Shanghai Key Discipline Construction Project, S30206；Shanghai Science and Technology Committee Foundation, 08DZ2271100

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摘要：

肿瘤细胞DNA修复能力与化疗药物敏感性密切相关，而DNA启动子甲基化可导致DNA修复相关基因转录失活、基因沉默、蛋白表达量改变等影响DNA的修复能力，继而导致肿瘤对化疗药物的固有性或获得性耐药。该文着重阐述DNA修复相关基因O6-甲基鸟嘌呤-DNA甲基转移酶（MGMT）、人类mut1同源物（hMLH1）和范科尼贫血互补基团F （FANCF）启动子甲基化与肿瘤化疗耐药之间的关系。

关键词: 启动子甲基化, DNA修复, 耐药, 烷化剂, O6-甲基鸟嘌呤-DNA甲基转移酶, 人类mut1同源物, 范科尼贫血互补基团F

Abstract:

The DNA repair ability of tumor cells is closely correlated with tumor chemosensitivity.  Promoter methylation of DNA may lead to transcriptional inactivation, gene silence and alteration of protein expression of DNA repair related genes, which in turn influences the ability of DNA repair, and therefore leads to the intrinsic and acquired tumor chemoresistance. This article briefly summaries the relationship between tumor chemoresistance and promoter methylation of DNA repair related genes such as O6-Methylguanine-DNA methyltransferase (MGMT), human mutL homologue 1 (hMLH1) and Fanconi anemia complementation group F (FANCF).

Key words: promoter methylation, DNA repair, chemoresistance, alkylating agents, O6-methylguanine-DNA methyltransferase, Fanconi anemia complementation group F