Triple kill: DDR inhibitors, radiotherapy and immunotherapy leave cancer cells with no escape

DNA损伤 癌症研究 DNA修复 免疫疗法 放射治疗 敏化 癌症 聚ADP核糖聚合酶 细胞周期检查点 医学 细胞周期 生物 免疫系统 免疫学 DNA 内科学 遗传学 聚合酶
作者
Yuyue Qiu,Xinru Hu,Xiaoping Zeng,Hongmei Wang
出处
期刊:Acta Biochimica et Biophysica Sinica [Oxford University Press]
卷期号:54 (11): 1569-1576 被引量:9
标识
DOI:10.3724/abbs.2022153
摘要

Radiotherapy (RT) has been widely used in the clinical treatment of cancers, but radiotherapy resistance (RR) leads to RT failure, tumor recurrence and metastasis. Many studies have been performed on the potential mechanisms behind RR, and a strong link has been found between RR and DNA damage. RT-induced DNA damage triggers a protective mechanism called the DNA damage response (DDR). DDR consists of several aspects, including the detection of DNA damage and induction of cell cycle checkpoint, DNA repair, and eventual induction of cell death. A large number of studies have shown that DDR inhibition leads to significantly enhanced sensitivity of cancer cells to RT. DDR may be an effective target for radio- and chemo-sensitization during cancer treatment. Therefore, many inhibitors of important enzymes involved in the DDR have been developed, such as PARP inhibitors, DNA-PK inhibitors, and ATM/ATR inhibitors. In addition, DNA damage also triggers the cGAS-STING signaling pathway and the ATM/ATR (CHK)/STAT pathway to induce immune infiltration and T-cell activation. This review discusses the effects of DDR pathway dysregulation on the tumor response to RT and the strategies for targeting these pathways to increase tumor susceptibility to RT. Finally, the potential for the combination treatment of radiation, DDR inhibition, and immunotherapy is described.
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