一个由EMP2控制的细胞周期依赖性铁灭敏感性开关.
Jason Rodencal1, Nathan Kim1, Veronica L Li2
1Department of Biology, Stanford University, Stanford, CA 94305, USA.
bioRxiv : the preprint server for biology
|July 28, 2023
概括
细胞循环停止增加了对GPX4抑制引起的铁亡的敏感性,而不是系统xc-抑制. 这种情况是由于受氧化脂在停止的细胞中增加.
科学领域:
- 细胞生物学 细胞生物学
- 生物化学 生物化学
- 在瘤学瘤学.
背景情况:
- 铁亡是一种受调节的细胞死亡途径,由依赖铁的脂质过氧化驱动.
- 它可以通过抑制囊/谷氨酸抗载体 (系统xc-) 或谷氨过氧化酶4 (GPX4) 来触发.
- 基于诱导方法,不同的调节机制可能会控制铁亡的敏感性.
结论:
- 细胞周期状态根据诱导剂不同调节铁灭的敏感性.
- 抑制GPX4诱导的铁亡是通过细胞周期依赖的脂质代谢和EMP2表达的变化来调节的.
- 这些发现表明,通过操纵细胞周期状态来向铁亡的潜在治疗策略.
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