TSC突变的肿瘤通过NRF2和谷胱甘肽耗竭对CDK7抑制敏感

The Tokushima journal of experimental medicine Pub Date : 2019-09-10 DOI:10.1084/jem.20190251

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

摘要

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。

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

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.

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The Tokushima journal of experimental medicine

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