Transcription factors in ferroptotic cell death.,Cancer Gene Therapy

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Transcription factors in ferroptotic cell death.
Cancer Gene Therapy ( IF 4.8 ) Pub Date : 2020-03-03 , DOI: 10.1038/s41417-020-0170-2
Chongshan Dai ₁ , Xin Chen ₁ , Jingbo Li ₁ , Paul Comish ₁ , Rui Kang ₁ , Daolin Tang ₁

Affiliation

Ferroptosis, a form of regulated cell death, is characterized by an excessive degree of iron accumulation and lipid peroxidation. Although it was originally identified only in cells expressing a mutant RAS oncogene, ferroptosis has also been found in normal cells following treatment by small molecules (e.g., erastin and RSL3) or drugs (e.g., sulfasalazine, sorafenib, and artesunate), which target antioxidant enzyme systems, especially the amino acid antiporter system xc- and the glutathione peroxidase GPX4. Dysfunctional ferroptosis is implicated in various physiological and pathological processes (e.g., metabolism, differentiation, and immunity). Targeting the ferroptotic network appears to a new treatment option for diseases or pathological conditions (e.g., cancer, neurodegeneration, and ischemia reperfusion injury). While the molecular machinery of ferroptosis remains largely unknown, several transcription factors (e.g., TP53, NFE2L2/NRF2, ATF3, ATF4, YAP1, TAZ, TFAP2C, SP1, HIF1A, EPAS1/HIF2A, BACH1, TFEB, JUN, HIC1, and HNF4A) play multiple roles in shaping ferroptosis sensitivity through either transcription-dependent or transcription-independent mechanisms. In this review, we summarize recent progress in understanding the transcriptional regulation underlying ferroptotic cell death, and discuss how it has provided new insights into cancer therapy.

中文翻译：

铁死亡细胞死亡中的转录因子。

铁死亡是一种受调节的细胞死亡形式，其特征是铁积累过多和脂质过氧化。尽管最初仅在表达突变 RAS 致癌基因的细胞中发现铁死亡，但在用靶向抗氧化剂的小分子（例如，erastin 和 RSL3）或药物（例如，柳氮磺吡啶、索拉非尼和青蒿琥酯）治疗后，正常细胞中也发现了铁死亡酶系统，尤其是氨基酸逆向转运蛋白系统 xc- 和谷胱甘肽过氧化物酶 GPX4。功能障碍性铁死亡与各种生理和病理过程（例如，代谢、分化和免疫）有关。针对铁死亡网络似乎是疾病或病理状况（例如，癌症、神经变性和缺血再灌注损伤）的新治疗选择。虽然铁死亡的分子机制在很大程度上仍然未知，但几种转录因子（例如，TP53、NFE2L2/NRF2、ATF3、ATF4、YAP1、TAZ、TFAP2C、SP1、HIF1A、EPAS1/HIF2A、BACH1、TFEB、JUN、HIC1 和 HNF4A ) 通过转录依赖性或转录非依赖性机制在塑造铁死亡敏感性方面发挥多种作用。在这篇综述中，我们总结了在理解铁死亡细胞死亡的转录调控方面的最新进展，并讨论了它如何为癌症治疗提供了新的见解。和 HNF4A）通过转录依赖性或转录非依赖性机制在塑造铁死亡敏感性方面发挥多种作用。在这篇综述中，我们总结了在理解铁死亡细胞死亡的转录调控方面的最新进展，并讨论了它如何为癌症治疗提供了新的见解。和 HNF4A）通过转录依赖性或转录非依赖性机制在塑造铁死亡敏感性方面发挥多种作用。在这篇综述中，我们总结了在理解铁死亡细胞死亡的转录调控方面的最新进展，并讨论了它如何为癌症治疗提供了新的见解。

更新日期：2020-04-24

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