铁死亡和结直肠癌中的肠道微生物代谢。
Gut microbial metabolism in ferroptosis and colorectal cancer.
发表日期：2024 Sep 10
作者：
Weiwei Cui, Meng Hao, Xin Yang, Chengqian Yin, Bo Chu
来源：
TRENDS IN CELL BIOLOGY
摘要：
铁死亡是由铁驱动的脂质过氧化诱导的程序性细胞死亡。大量研究表明，铁死亡与结直肠癌 (CRC) 的进展有关，并已成为对抗治疗耐药性 CRC 的一种有前景的策略。虽然 CRC 细胞的内在抗铁死亡和促铁死亡途径已得到很好的表征，但在 CRC 发病机制中调节铁死亡的外在代谢途径仍知之甚少。新的证据表明肠道微生物代谢与结直肠癌的进展密切相关。这篇综述概述了肠道微生物代谢，并讨论了这些源自肠道微生物群的代谢物如何通过铁死亡促进癌症可塑性。针对肠道微生物介导的铁死亡是治疗 CRC 的一种潜在方法。版权所有 © 2024 Elsevier Ltd. 保留所有权利。
Ferroptosis is programmed cell death induced by iron-driven lipid peroxidation. Numerous studies have shown that ferroptosis is implicated in the progression of colorectal cancer (CRC) and has emerged as a promising strategy to combat therapy-resistant CRC. While the intrinsic antiferroptotic and proferroptotic pathways in CRC cells have been well characterized, extrinsic metabolism pathways regulating ferroptosis in CRC pathogenesis remain less understood. Emerging evidence shows that gut microbial metabolism is tightly correlated with the progression of CRC. This review provides an overview of gut microbial metabolism and discusses how these metabolites derived from intestinal microflora contribute to cancer plasticity through ferroptosis. Targeting gut microbe-mediated ferroptosis is a potential approach for CRC treatment.Copyright © 2024 Elsevier Ltd. All rights reserved.