Wang Ziyi, Jia Renxiang, Wang Linlin, Yang Qiwei, Hu Xiaohai, Fu Qiang, Zhang Xinyu, Li Wenya, Ren Yi
Department of Thoracic Surgery, Shenyang Chest Hospital & Tenth People's Hospital, Shenyang, China.
Department of Thoracic Surgery, First Affiliated Hospital of China Medical University, Shenyang, China.
Front Oncol. 2022 Jul 7;12:935593. doi: 10.3389/fonc.2022.935593. eCollection 2022.
Defects in DNA repair pathways are emerging hallmarks of cancer. Accurate DNA repairs and replications are essential for genomic stability. Cancer cells require residual DNA repair capabilities to repair the damage from replication stress and genotoxic anti-tumor agents. Defective DNA repair also promotes the accumulation of genomic changes that eventually lead to tumorigenesis, tumor progression, and therapeutic resistance to DNA-damaging anti-tumor agents. Rad51 recombinase is a critical effector of homologous recombination, which is an essential DNA repair mechanism for double-strand breaks. Rad51 has been found to be upregulated in many malignant solid tumors, and is correlated with poor prognosis. In multiple tumor types, Rad51 is critical for tumor metabolism, metastasis and drug resistance. Herein, we initially introduced the structure, expression pattern of Rad51 and key Rad51 mediators involved in homologous recombination. Additionally, we primarily discussed the role of Rad51 in tumor metabolism, metastasis, resistance to chemotherapeutic agents and poly-ADP ribose polymerase inhibitors.
DNA修复途径缺陷是癌症新出现的特征。准确的DNA修复和复制对于基因组稳定性至关重要。癌细胞需要残余的DNA修复能力来修复复制应激和基因毒性抗肿瘤药物造成的损伤。有缺陷的DNA修复还会促进基因组变化的积累，最终导致肿瘤发生、肿瘤进展以及对DNA损伤抗肿瘤药物产生治疗抗性。Rad51重组酶是同源重组的关键效应因子，同源重组是双链断裂的一种重要DNA修复机制。已发现Rad51在许多恶性实体瘤中上调，且与预后不良相关。在多种肿瘤类型中，Rad51对肿瘤代谢、转移和耐药性至关重要。在此，我们首先介绍了Rad51的结构、表达模式以及参与同源重组的关键Rad51介质。此外，我们主要讨论了Rad51在肿瘤代谢、转移、对化疗药物和聚ADP核糖聚合酶抑制剂耐药性方面的作用。
