Engaged for survival: From cadherin ligation to STAT3 activation.

JAK-STAT Pub Date : 2013-10-01 Epub Date: 2013-12-06 DOI:10.4161/jkst.27363
Mulu Geletu, Stephanie Guy, Rozanne Arulanandam, Hélène Feracci, Leda Raptis
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引用次数: 21

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.

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参与生存:从钙粘蛋白连接到STAT3激活。
在正常组织或肿瘤中,细胞有广泛的机会与邻近细胞粘附。这种状态被密集的细胞培养所模拟。在这篇综述中,我们整合了一些关于关键信号换能器STAT3(信号换能器和转录激活器-3)的最新发现,STAT3的活性在钙粘蛋白介导的细胞间粘附后急剧增加。钙粘蛋白参与,在密集细胞培养中更受青睐,通过抑制蛋白酶体降解导致总Rac/Cdc42蛋白水平的急剧增加,随后是IL-6和STAT3的激活。cadherin/Rac/IL-6/STAT3轴提供了一个有效的生存信号,这是肿瘤转化和正常组织功能的先决条件。
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