G3BP1 耗竭通过诱导氧化应激来增加对 DNA 损伤的放射敏感性。
G3BP1 Depletion Increases Radiosensitisation by Inducing Oxidative Stress in Response to DNA Damage.
机构信息
Team of Radiation Convergence Research, Korea Institute of Radiological and Medical Sciences, Seoul, Republic of Korea.
Division of Radiation Biomedical Research, Korea Institute of Radiological and Medical Sciences, Seoul, Republic of Korea.
出版信息
Anticancer Res. 2019 Nov;39(11):6087-6095. doi: 10.21873/anticanres.13816.
BACKGROUND
RAS GTPase-activating protein-binding protein (G3BP1) is an RNA-binding protein that is essential for assembling stress granules. Many functions related to the survival and progression of cancer have been reported. The current study aimed to investigate the role of G3BP1 in radio-sensitisation of cancer cells.
MATERIALS AND METHODS
Radiation sensitivity and chemosensitivity were analysed in A549 and H460 cells transfected with G3BP1 siRNAs, and N-acetyl-L-cysteine (NAC) was used to elucidate the involvement of reactive oxygen species (ROS).
RESULTS
G3BP1 depletion sensitised lung cancer cell lines to radiation, and the effect was related to ROS. G3BP1 depletion impaired the intracellular ROS scavenging system and NAC abolished the radiation-sensitive phenotypes caused by G3BP1 depletion.
CONCLUSION
The study suggested G3BP1 as a promising target for radio- and chemosensitisation of lung cancer.
背景
RAS GTP 酶激活蛋白结合蛋白（G3BP1）是一种 RNA 结合蛋白，对于组装应激颗粒至关重要。已经报道了许多与癌症的生存和进展相关的功能。本研究旨在探讨 G3BP1 在癌细胞放射增敏中的作用。
材料和方法
用 G3BP1 siRNA 转染 A549 和 H460 细胞，分析其辐射敏感性和化疗敏感性，并使用 N-乙酰-L-半胱氨酸（NAC）阐明活性氧（ROS）的参与。
结果
G3BP1 耗竭使肺癌细胞系对辐射敏感，其作用与 ROS 有关。G3BP1 耗竭破坏了细胞内 ROS 清除系统，NAC 消除了 G3BP1 耗竭引起的辐射敏感表型。
结论
该研究表明 G3BP1 是肺癌放射增敏和化疗增敏的有前途的靶点。
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