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首页> 外文期刊>Journal of Cellular Physiology >A novel role of ERK5 in integrin-mediated cell adhesion and motility in cancer cells via Fak signaling.
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A novel role of ERK5 in integrin-mediated cell adhesion and motility in cancer cells via Fak signaling.

机译：一本小说ERK5 integrin-mediated细胞的作用通过Fak癌细胞粘附和能动性信号。

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摘要

In metastatic cancer, high expression levels of vitronectin (VN) receptors (integrins), FAK, and ERK5 are reported. We hypothesized that integrin-mediated ERK5 activation via FAK may play a pivotal role in cell adhesion, motility, and metastasis. ERK5 and FAK phosphorylation when metastatic MDA-MB-231 and PC-3 cells were plated on VN was enhanced. Further experiments showed co-immunoprecipitation of integrins beta1, alpha V beta 3, or alpha V beta 5 with ERK5 and FAK. To gain better insight into the mechanism of ERK5, FAK, and VN receptors in cell adhesion and motility, we performed loss-of-function experiments using integrin blocking antibodies, and specific mutants of FAK and ERK5. Ectopic expression of dominant negative ERK5/AEF decreased ERK5 and FAK (Y397) phosphorylation, cell adhesion, and haptotactic motility (micromotion) on VN. Additionally, DN FAK expression attenuated ERK5 phosphorylation, cell adhesion, and motility. This study documents the novel finding that in breast and prostate cancercells, ERK5 is a critical target of FAK in cell adhesion signaling. Using different cancer cells, our experiments unveil a novel mechanism by which VN receptors and FAK could promote cancer metastasis via ERK5 activation.
机译：在转移性癌症,高水平的表达vitronectin (VN)受体(整合),FAK,ERK5报告。通过FAK integrin-mediated ERK5激活在细胞粘附、运动中发挥关键作用,和转移。转移性mda - mb - 231和曲泽细胞被镀VN增强。整合素beta1 co-immunoprecipitation,αV Vβ3或αβ5 ERK5和FAK。更深入地了解ERK5的机制,FAK, VN受体在细胞粘附和能动性,我们执行功能丧失实验使用整合素阻止抗体,和特定的突变体的FAK和ERK5。显性负ERK5 /时的表情ERK5和降低FAK磷酸化(Y397),细胞粘附,haptotactic能动性(微动)VN。减毒ERK5磷酸化表达,细胞附着力和能动性。小说中发现乳腺癌和前列腺癌cancercells, ERK5 FAK的关键目标细胞粘附信号。细胞,我们的实验推出一个新颖的机制VN受体和FAK可以促进通过ERK5激活癌症转移。

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