DNA损伤应答与细胞老化及癌变机制研究进展

发布时间：2018-10-29 15:26

【摘要】：目的 DNA损伤是引起细胞老化的主要原因,细胞老化与肿瘤的发生发展密切相关。本研究旨在探讨DNA损伤应答和磷酸肌醇生物合成通路调控细胞老化及肿瘤发生的机制。方法以"肿瘤、DNA损伤、细胞老化和磷酸肌醇"等为关键词,检索PubMed、中国知网和万方数据库2000-01-2016-07的相关文献。纳入标准:(1)涉及到DNA损伤与细胞老化和肿瘤之间的相关性;(2)与磷酸肌醇生物合成通路对细胞老化和肿瘤的调控有关;(3)论述了细胞老化的相关表型及其产生机制。根据纳入标准,符合分析的文献42篇。结果 DNA损伤主要通过p53/p21、p16INK4a/pRB以及GATA4通路调控细胞老化进程。磷酸肌醇生物合成通路中的一些分子和蛋白激酶,如IP6、IP7和IP6K等也参与DNA损伤修复的调控,影响细胞老化及肿瘤发生。细胞老化既可以抑制肿瘤的发生也可以促进肿瘤的发生。结论DNA损伤应答和磷酸肌醇生物合成通路通过多种途径调控细胞老化及肿瘤的发生,为肿瘤的防治提供了新靶点。
[Abstract]:Objective DNA damage is the main cause of cell aging, and cell aging is closely related to the occurrence and development of tumor. The aim of this study was to investigate the mechanisms of DNA damage response and inositol phosphate biosynthesis pathway regulating cell aging and tumorigenesis. Methods using "tumor, DNA damage, cell aging and inositol phosphate" as the key words, the relevant literatures of PubMed, and Wanfang database 2000-01-2016-07 were searched. The inclusion criteria were as follows: (1) the correlation between DNA damage and cell aging and tumor, (2) the regulation of inositol phosphate biosynthesis pathway on cell aging and tumor; (3) the phenotypes and mechanism of cell aging were discussed. According to the inclusion criteria, 42 articles were analyzed. Results DNA damage regulated the process of cell aging mainly through p53 / p21 p16INK4a / PRRB and GATA4 pathway. Some molecules and protein kinases in inositol phosphate biosynthesis pathway, such as IP6,IP7 and IP6K, are also involved in the regulation of DNA damage and repair, affecting cell aging and tumorigenesis. Cell aging can not only inhibit the occurrence of tumor, but also promote the occurrence of tumor. Conclusion DNA damage response and inositol phosphate biosynthesis pathway regulate cell aging and tumorigenesis through a variety of pathways, which provide a new target for the prevention and treatment of tumor.
【作者单位】：哈尔滨医科大学基础医学院医学遗传学研究室;哈尔滨医科大学附属第二医院妇产科;
【基金】：国家自然科学基金(81272582)
【分类号】：R730.2

【相似文献】