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表皮-介质细胞过渡促进了代谢重编程以抑制铁灭症

Wenzheng Guo¹, Zhibing Duan¹, Jingjing Wu¹

¹Departments of Molecular and Cellular Biochemistry, and the Markey Cancer Center, College of Medicine, University of Kentucky, Lexington, KY 40506, United States.

Seminars in cancer biology

|March 9, 2025

概括

表皮-介质细胞过渡 (EMT) 增加了癌细胞的可塑性和转移. 此外,EMT还会触发新陈代谢变化以抵抗细胞死亡途径铁亡,从而提供新的治疗点.

科学领域:

癌症生物学癌症生物学
细胞可塑性细胞可塑性
代谢调节代谢调节代谢调节

背景情况:

表皮-介质细胞过渡 (EMT) 对于发育和转移至关重要,赋予茎状特征和形态变化.
EMT涉及细胞骨重组和由于多不和脂肪酸 (PUFA) 的膜刚性降低,增强细胞运动性.
高水平的PUFA增加了对脂质过氧化和ferroptosis的敏感性,这是一个受调节的细胞死亡途径.

研究的目的:

总结最近关于EMT,脂质代谢和铁亡之间的相互作用的发现.
讨论这些相互作用如何调节转移性癌细胞中的细胞可塑性和铁灭性抵抗.
探索针对这些途径的潜在治疗干预措施.

主要方法:

文献综述和当前研究结果的综合.
分析 EMT,脂质代谢和铁化之间的分子机制.
在EMT和ferroptosis缓解中讨论表观遗传调节.

主要成果:

通过改变膜性质,EMT可以增强细胞可塑性和转移潜力.
代谢重编程,特别是在脂质代谢中,是由EMT诱导的,以抵消ferroptosis.
表观遗传机制在调节EMT和减轻ferroptosis诱导的损害方面发挥着作用.

结论:

在EMT,脂质代谢和铁化之间的复杂相互作用代表了癌症转移中的关键调节层.
了解这些相互作用提供了关于细胞可塑性和铁灭抵抗性的见解.
针对这些途径为新的癌症治疗策略提供了有希望的途径.

关键词:

在EMT中,EMT是EMT.铁化是铁化的一种.脂质代谢脂质代谢是一种膜的可塑性膜的可塑性转移转移转移转移

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