RAC1在MET驱动的非锚定依赖肿瘤生长中的非常规作用。

Unconventional role of RAC1 in MET-driven anchorage-independent tumor growth.

作者信息

Hervieu Alexia, Kermorgant Stéphanie

机构信息

Spatial Signalling Team, Barts Cancer Institute, Queen Mary University of London, John Vane Science Centre, London, UK.

Signal Transduction and Molecular Pharmacology Team, CRUK Cancer Therapeutics Unit, Division of Cancer Therapeutics, Institute of Cancer Research, London, UK.

出版信息

Mol Cell Oncol. 2020 Aug 18;7(6):1803029. doi: 10.1080/23723556.2020.1803029.

DOI:10.1080/23723556.2020.1803029

PMID:33235904

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7671004/

Abstract

We reported that RAC1 is a master regulator of cell migration and anchorage-independent growth, downstream of the oncogenic Receptor Tyrosine Kinase (RTK) MET. RAC1 growth-promoting role is guanosine triphosphatase (GTPase)- and phosphatidylinositol 3-kinase (PI3K)-independent but promotes mammalian target of rapamycin (mTOR) signaling through triggering its plasma membrane localization.

摘要

我们报道，RAC1是细胞迁移和不依赖贴壁生长的主要调节因子，位于致癌受体酪氨酸激酶（RTK）MET的下游。RAC1的促生长作用不依赖鸟苷三磷酸酶（GTPase）和磷脂酰肌醇3激酶（PI3K），但通过触发其质膜定位促进雷帕霉素哺乳动物靶蛋白（mTOR）信号传导。