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敲低 RAB25 促进卵巢癌细胞自噬并抑制细胞生长。

Knockdown of RAB25 promotes autophagy and inhibits cell growth in ovarian cancer cells.

机构信息

Obstetrics and Gynecology Hospital of Fudan University, Shanghai 200011, PR China.

出版信息

Mol Med Rep. 2012 Nov;6(5):1006-12. doi: 10.3892/mmr.2012.1052. Epub 2012 Aug 28.

Abstract

RAB25 belongs to the Rab family of small GTPases and is implicated in the development of various types of human cancer. To evaluate the role of RAB25 in ovarian cancer, RAB25 was knocked down by siRNA in HEY and ES‑2 human ovarian cancer cells. Autophagy, cell growth and cell apoptosis were evaluated. The results showed that knockdown of RAB25 increased acidic vesicle organelles and GFP-microtubule-associated protein 1 light chain 3 punctate fluorescence in ovarian cancer cells. Autophagy that promoted by knockdown of RAB25 was not observed in cells where the ERK1/2 signaling pathway had been inhibited by U0126. Knockdown of RAB25 reduced cell cycle progression and cell growth. Apoptosis of ovarian cancer cells could be induced by knockdown of RAB25. These results support the tumorigenic role of RAB25 in ovarian cancer cells.

摘要

RAB25 属于 Rab 家族的小 GTPases,与多种类型的人类癌症的发生有关。为了评估 RAB25 在卵巢癌中的作用,本研究通过 siRNA 敲低 HEY 和 ES-2 人卵巢癌细胞中的 RAB25。评估自噬、细胞生长和细胞凋亡。结果表明,敲低 RAB25 增加了卵巢癌细胞中的酸性囊泡细胞器和 GFP-微管相关蛋白 1 轻链 3 点状荧光。在 ERK1/2 信号通路被 U0126 抑制的细胞中,未观察到由 RAB25 敲低促进的自噬。敲低 RAB25 减少细胞周期进程和细胞生长。RAB25 的敲低可诱导卵巢癌细胞凋亡。这些结果支持 RAB25 在卵巢癌细胞中的致瘤作用。

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