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首页> 外文期刊>Journal of cellular physiology. >Elucidation of the mechanism underlying CD44v6-induced transformation of IEC-6 normal intestinal epithelial cells
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Elucidation of the mechanism underlying CD44v6-induced transformation of IEC-6 normal intestinal epithelial cells

机译：机制的说明CD44v6-induced IEC-6转换正常肠上皮细胞

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摘要

The transformation abilities of CD44s and CD44v6 in normal intestinal epithelial cells have not yet been reported. Herein, we established both CD44s and CD44v6 over-expressing stable clones from rat IEC-6 cells and demonstrated that the CD44v6 clones had higher saturation density and anchorage independence. Additionally, CD44v6 clones were more resistant to oxaliplatin and irinotecan which might be attributed to a significantly increased B-cell lymphoma 2 level and a reduced DNA damage response in these cells. Moreover, c-Met and vascular endothelial growth factor receptor 2 signalings were involved in modulating the saturation density in CD44v6 clones. Interestingly, higher activation of both AKT and extracellular-signal-regulated kinase (ERK) were detected in CD44v6 clones which might account in part for the cell density-independent nuclear localization of Yes-associated protein (YAP). To no surprise, increases of both saturation density and anchorage independence in CD44v6 clones were markedly diminished by PI3K, AKT, MEK, and ERK inhibitors as well as YAP knockdown. By contrast, overexpression of a constitutively active YAP robustly increased the aforementioned phenotypes in IEC-6 cells. Collectively, our results suggest that upregulation of CD44v6, but not CD44s, induces the transformation of normal intestinal epithelial cells possibly via activating the c-Met/AKT/YAP pathway which might also explain the important role of CD44v6 in the initiation of various carcinomas.
机译：cd44和CD44v6的转换能力在正常肠上皮细胞没有未报道。cd44和CD44v6过度表达稳定的克隆从老鼠IEC-6细胞并证明了CD44v6克隆饱和密度和较高安克雷奇的独立性。克隆对铂有抵抗力伊立替康可能归因于一个显著增加b细胞淋巴瘤2水平和降低这些细胞DNA损伤反应。此外,c-Met和血管内皮生长因子受体2信号参与调制CD44v6的饱和密度克隆。一种蛋白激酶和extracellular-signal-regulated激酶(ERK)检测CD44v6克隆这可能细胞密度独立账户部分核本地化Yes-associated蛋白质(废话)。饱和密度和锚固独立CD44v6克隆被PI3K明显减弱,一种蛋白激酶,MEK和ERK抑制剂以及狂吠可拆卸的。持续活跃YAP强劲增加提到的IEC-6细胞表型。总的来说,我们的研究结果表明,upregulation CD44v6、但不是cd44,诱发正常肠道的变换上皮细胞可能通过激活c-Met / AKT YAP途径也可以解释CD44v6在起始的重要作用各种癌。

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