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首页> 外文期刊>Journal of Cellular Physiology >Butyrate-treated colonic Caco-2 cells exhibit defective integrin-mediated signaling together with increased apoptosis and differentiation.
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Butyrate-treated colonic Caco-2 cells exhibit defective integrin-mediated signaling together with increased apoptosis and differentiation.

机译：Butyrate-treated结肠Caco-2细胞展览缺陷integrin-mediated信号一起增加细胞凋亡和分化。

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摘要

We previously reported that the enterocytic differentiation of human colonic Caco-2 cells correlated with alterations in integrin signaling. We now investigated whether differentiation and apoptosis of Caco-2 cells induced by the short-chain fatty acid butyrate (NaBT) was associated with alterations in the integrin-mediated signaling pathway with special interest in the expression and activity of focal adhesion kinase (FAK), of the downstream phosphatidylinositol 3'-kinase (PI 3-kinase)-Akt pathway and in the role of the nuclear factor kappaB (NF-kappaB). NaBT increased the level of sucrase. It induced apoptosis as shown by: (1) decreased Bcl-2 and Bcl-X(L) proteins and increased Bax protein; (2) activation of caspase-3; and (3) increased shedding of apoptotic cells in the medium. This effect was associated with defective integrin-mediated signaling as shown by: (1) down-regulation of beta1 integrin expression; 2) decreased FAK expression and tyrosine phosphorylation; (3) concerted alterations in cytoskeletal and structural focal adhesions proteins (talin, ezrin); and (4) decreased FAK ability to associate with PI 3-kinase. However, in Caco-2 cells, beta1-mediated signaling failed to be activated downstream of FAK and PI 3-kinase at the level of Akt. Transfection studies show that NaBT treatment of Caco-2 cells promoted a significant activation of the NF-kappaB which was probably involved in the NaBT-induced apoptosis. Our results indicate that the prodifferentiating agent NaBT induced apoptosis of Caco-2 cells probably through NF-kappaB activation together with a defective beta1 integrin-FAK-PI 3-kinase pathways signaling. J. Cell. Physiol. 197: 336-347, 2003Copyright 2003 Wiley-Liss, Inc.
机译：我们以前报道,enterocytic人类结肠Caco-2细胞的分化整合素与改变信号。Caco-2细胞的分化和凋亡短链脂肪酸丁酸诱导(NaBT)的改变有关integrin-mediated信号通路与特别焦的表达和活动的兴趣下游的黏附激酶(FAK)一种蛋白激酶磷脂酰肌醇3激酶(π3-kinase)途径和核转录因子的作用kappaB (NF-kappaB)。蔗糖酶。蛋白质和bcl - 2和减少Bcl-X (L)伯灵顿蛋白增加;caspase-3;在中凋亡细胞。与缺陷integrin-mediated信号如图所示:(1)下调beta1整合素表达;表达及酪氨酸磷酸化;共同改变细胞骨架结构局部粘连蛋白(蛋白,ezrin);和π3-kinase交往。细胞,beta1-mediated信号失败激活下游FAK和π3-kinase一种蛋白激酶的水平。NaBT Caco-2细胞晋升待遇的NF-kappaB显著激活可能参与NaBT-induced细胞凋亡。我们的结果表明,prodifferentiating代理NaBT Caco-2细胞的诱导细胞凋亡可能通过NF-kappaB激活起来与一个有缺陷的beta1 integrin-FAK-PI 3-kinase通路的信号。336 - 347年,2003年版权2003年Wiley-Liss公司。

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