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在卵巢癌中,Ets1通过Drp1介导的线粒体碎片化促进EMT/入侵

Deepshikha Ghosh¹, Suman Pakhira¹, Damayanti Das Ghosh²

¹Cell Biology and Physiology Division, CSIR Indian Institute of Chemical Biology (CSIR IICB), 4, Raja S.C. Mullick Road, Kolkata 700032, India.

|September 4, 2023

概括

通过改变线粒体动态和能量生产,Ets1促进卵巢癌的进展. 抑制Drp1-介导的线粒体裂变减少了Ets1-驱动的癌细胞入侵和上皮转移到介质细胞 (EMT).

科学领域:

在瘤学瘤学.
细胞生物学细胞生物学
生物化学生物化学

背景情况:

卵巢癌是女性癌症死亡的主要原因,原因是其侵略性和缺乏早期检测方法.
Ets1coprotein与促进表皮细胞转移到介质细胞转变 (EMT) 有关,并作为卵巢癌中的潜在恶性瘤标记物.

研究的目的:

研究Ets1在调节卵巢癌中线粒体动力学和生物能学的作用.
为了确定是否准线粒体裂变可以减轻Ets1驱动的EMT和入侵.

主要方法:

研究了Ets1通过Drp1 (DNM1L) 促进体结合来调节线粒体裂变-融合动态.
评估了线粒体负载,OXPHOS复合体5 (ATP合成酶) 表达和生物能量转变 (糖解与OXPHOS).
评估了Drp1抑制对Ets1相关EMT的试验室和体内效应,使用合成基因小鼠模型.

主要成果:

过度表达Ets1会增加Drp1,导致线粒体碎片化和线粒体质量减少.
这种碎片化损害了OXPHOS复合体5的表达,促进了氧化酸化的糖解.
抑制Drp1-介导的线粒体裂变有效地减少了Ets1-驱动的EMT和细胞培养和小鼠模型中的入侵.

结论:

通过通过Drp1-介导的裂变改变线粒体的生物能学,Ets1驱动卵巢癌的进展.
针对Drp1-介导的线粒体碎片化是一种潜在的治疗策略,可以抑制Ets1-驱动的EMT和卵巢癌的入侵.

关键词:

癌症癌症癌症癌症分子生物学分子生物学

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