为生存而参与：从钙黏蛋白连接到信号转导及转录激活因子3激活。
Engaged for survival: From cadherin ligation to STAT3 activation.
作者信息
Geletu Mulu, Guy Stephanie, Arulanandam Rozanne, Feracci Hélène, Raptis Leda
机构信息
Department of Pathology; Queen's University; Kingston, ON Canada.
Université Bordeaux 1; Centre de Recherche Paul Pascal; CNRS UPR 8641; Pessac, France.
出版信息
JAKSTAT. 2013 Oct 1;2(4):e27363. doi: 10.4161/jkst.27363. Epub 2013 Dec 6.
Abstract
In normal tissues or tumors, cells have extensive opportunities for adhesion to their neighbors. This state is mimicked by dense cell cultures. In this review, we integrate some recent findings on a key signal transducer, STAT3 (signal transducer and activator of transcription-3), whose activity is dramatically increased following cadherin-mediated cell to cell adhesion. Cadherin engagement, favored in dense cell cultures, causes a dramatic increase in total Rac/Cdc42 protein levels through inhibition of proteasomal degradation, which is followed by activation of IL-6 and STAT3. The cadherin/Rac/IL-6/STAT3 axis offers a potent survival signal that is a prerequisite for neoplastic transformation, as well as normal tissue function.
摘要
在正常组织或肿瘤中，细胞有大量机会与相邻细胞黏附。这种状态在高密度细胞培养中得以模拟。在本综述中，我们整合了一些关于关键信号转导子STAT3（信号转导与转录激活因子3）的最新研究发现，其活性在钙黏蛋白介导的细胞间黏附后会显著增加。在高密度细胞培养中有利于发生的钙黏蛋白结合，通过抑制蛋白酶体降解导致Rac/Cdc42总蛋白水平显著升高，随后激活白细胞介素-6和STAT3。钙黏蛋白/Rac/白细胞介素-6/STAT3轴提供了一种强大的生存信号，这是肿瘤转化以及正常组织功能的先决条件。
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