肿瘤防治研究2024，Vol.51Issue(7)：600-605,6.DOI:10.3971/j.issn.1000-8578.2024.23.1198
细胞核遗传物质损伤后癌细胞最终命运走向分析
Final Fate of Cancer Cells After Nuclear Genetic Material Damage
摘要
Abstract
Cancer cells refer to a group of malignant cells with strong division and proliferation abilities.Cancer cells rely on the unstable plunder of human nutrition to sustain the large amount of energy that they need for their own division and proliferation.The division and proliferation of cancer cells are linked to the synthesis and replication of genetic material in the nucleus.Blockage or destruction of the synthesis of genetic material in cancer cells is one of the mechanisms underlying the action of most antitumor drugs.As the key material that dominates cell division,proliferation,and death,nuclear genetic material which mainly refers to the deoxyribonucleic acid located on the chromatin in the nucleus,plays a decisive role in the final fate of cells.The final fate of cancer cells after the damage of the genetic material is worthy of investigation and analysis.In this paper,we discuss and analyze the fate of cancer cells after genetic material damage from the aspect of cellular cycle arrest,apoptosis,autophagy,and senescence to provide ideas for the mechanism research on antitumor drugs.关键词
遗传物质损伤/癌细胞/周期阻滞/凋亡/自噬/衰老Key words
Genetic material damage/Cancer cell/Cycle arrest/Apoptosis/Autophagy/Senescence分类
医药卫生引用本文复制引用
王磊,许小敏,王建,牟方政,魏大荣..细胞核遗传物质损伤后癌细胞最终命运走向分析[J].肿瘤防治研究,2024,51(7):600-605,6.基金项目
Luo Chang-yi National Famous Traditional Chinese Medicine Expert Inheritance Studio Construction Project(Management Measures for Education of Chinese Traditional Chinese Medicine Professional and Technical Personnel[2019]No.41) （Management Measures for Education of Chinese Traditional Chinese Medicine Professional and Technical Personnel[2019]No.41）
Chongqing Science and Health Joint Traditional Chinese Medicine Research Project(No.2024ZYQN014) 骆常义全国名老中医专家传承工作室建设项目(中国中医药专业技术人员师承教育管理办法函[2019]41号) （No.2024ZYQN014）
重庆市科卫联合中医药科研项目(2024ZYQN014) （2024ZYQN014）
