遗传 ›› 2022, Vol. 44 ›› Issue (6): 466-477.doi: 10.16288/j.yczz.22-067
赵岩1, 王晨鑫2(), 杨天明2, 李春爽2, 张丽宏2, 杜冬妮2, 王若曦3, 王静4, 魏民2, 巴雪青2()
收稿日期:
2022-03-10
修回日期:
2022-04-16
出版日期:
2022-06-20
发布日期:
2022-04-22
通讯作者:
巴雪青
E-mail:wangcx968@nenu.edu.cn;baxq755@nenu.edu.cn
作者简介:
赵岩,学士,副主任技师,研究方向:细胞生物学。E-mail: 基金资助:
Yan Zhao1, Chenxin Wang2(), Tianming Yang2, Chunshuang Li2, Lihong Zhang2, Dongni Du2, Ruoxi Wang3, Jing Wang4, Min Wei2, Xueqing Ba2()
Received:
2022-03-10
Revised:
2022-04-16
Online:
2022-06-20
Published:
2022-04-22
Contact:
Ba Xueqing
E-mail:wangcx968@nenu.edu.cn;baxq755@nenu.edu.cn
Supported by:
摘要:
有氧代谢有机体细胞无法避免活性氧(reactive oxygen species, ROS)的伤害。ROS会造成多种形式的DNA损伤,其中鸟嘌呤G的氧化产物8-羟鸟嘌呤(8-oxoG)是频度最高的一种DNA氧化损伤,由特异性的糖苷酶OGG1识别并开启碱基切除修复通路完成修复。8-oxoG如果没有及时修复,可能会在复制的过程中引入G:C配对到T:A配对的碱基颠换突变。因此8-oxoG的积累或OGG1修复功能异常被认为会影响基因功能,进而导致肿瘤或衰老相关疾病的发生,然而直接实验证据却极为有限。近年来一系列研究表明,8-oxoG倾向于产生在基因的调控区,在这种情形下,8-oxoG可视为一种表观遗传学修饰,而OGG1则是这一信息的特异性读取者,OGG1对底物的识别、结合或切除会引发DNA构象或组蛋白修饰的改变,进而引起基因表达的上调或下调。因此,除了潜在的遗传毒性,鸟嘌呤氧化损伤与肿瘤的关联与其通过表观遗传学机制引发基因表达的异常密切相关。本文对8-oxoG及修复酶OGG1与肿瘤发生发展的关联机制进行了分析与总结,旨在提示研究人员从新的视角解读DNA氧化损伤与肿瘤的关系,并为肿瘤的治疗提供新的思路和靶点。
赵岩, 王晨鑫, 杨天明, 李春爽, 张丽宏, 杜冬妮, 王若曦, 王静, 魏民, 巴雪青. DNA氧化损伤8-羟鸟嘌呤与肿瘤的发生发展[J]. 遗传, 2022, 44(6): 466-477.
Yan Zhao, Chenxin Wang, Tianming Yang, Chunshuang Li, Lihong Zhang, Dongni Du, Ruoxi Wang, Jing Wang, Min Wei, Xueqing Ba. Linking oxidative DNA lesion 8-OxoG to tumor development and progression[J]. Hereditas(Beijing), 2022, 44(6): 466-477.
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