粒体自噬
DNA损伤
自噬
细胞生物学
帕金
DNA修复
细胞周期
生物
癌细胞
抗辐射性
癌症研究
线粒体
程序性细胞死亡
癌症
细胞凋亡
DNA
细胞培养
遗传学
医学
病理
疾病
帕金森病
作者
Yanxian Ren,Pengfei Yang,Chenghao Li,Weihong Wang,Tianyi Zhang,Li Jin,H Li,Changfeng Dong,Wenbo Meng,Heng Zhou
标识
DOI:10.1038/s41420-023-01573-0
摘要
Radiotherapy is an important cancer treatment strategy that causes DNA damage in tumor cells either directly or indirectly. Autophagy is a physiological process linked to DNA damage. Mitophagy is a form of autophagy, which specifically targets and eliminates impaired mitochondria, thereby upholding cellular homeostasis. However, the connection between DNA damage and mitophagy has yet to be fully elucidated. We found that mitophagy, as an upstream signal, increases ionizing radiation-induced DNA damage by downregulating or overexpressing key mitophagy proteins Parkin and BNIP3. Enhancing the basal level of mitophagy in conjunction with X-ray irradiation can potentially diminish cell cycle arrest at the G2/M phase, substantially elevate the accumulation of γ-H2AX, 53BP1, and PARP1 foci within the nucleus, augment DNA damage, and facilitate the demise of tumor cells. Consequently, this approach prolongs the survival of melanoma-bearing mice. The findings of this study are anticipated to offer a therapeutic approach for enhancing the therapeutic effectiveness of radiotherapy.
科研通智能强力驱动
Strongly Powered by AbleSci AI