Tumors with TSC mutations are sensitive to CDK7 inhibition through NRF2 and glutathione depletion

Mahsa Zarei, H. Du, A. Nassar, Rachel E Yan, K. Giannikou, Sneha Johnson, H. Lam, E. Henske, Yubao Wang, Tinghu Zhang, J. Asara, D. Kwiatkowski
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引用次数: 15

Abstract

Tuberous sclerosis complex (TSC) is a genetic disorder in which tumors develop due to TSC1/TSC2 loss and activation of mTORC1. Zarei et al. show that TSC tumors are sensitive to CDK7 inhibition, which reduces expression of NRF2 and glutathione synthetic genes, leading to glutathione depletion and ROS-mediated cell death.
TSC突变的肿瘤通过NRF2和谷胱甘肽耗竭对CDK7抑制敏感
结节性硬化症(TSC)是一种由于TSC1/TSC2缺失和mTORC1激活而导致肿瘤发展的遗传性疾病。Zarei等研究表明,TSC肿瘤对CDK7抑制敏感,CDK7抑制可降低NRF2和谷胱甘肽合成基因的表达,导致谷胱甘肽耗损和ros介导的细胞死亡。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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