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首页> 外文期刊>Journal of Cellular Physiology >Y-box Binding Protein-1 Is Part of a Complex Molecular Network Linking Np63 to the PI3K/akt Pathway in Cutaneous Squamous Cell Carcinoma
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Y-box Binding Protein-1 Is Part of a Complex Molecular Network Linking Np63 to the PI3K/akt Pathway in Cutaneous Squamous Cell Carcinoma

机译：Y-box绑定蛋白1是一个复杂的一部分分子网络链接Np63 PI3K / akt在皮肤鳞状细胞癌途径

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Cutaneous squamous cell carcinomas (SCCs) typically lack somatic oncogene-activating mutations and most of them contain p53 mutations. However, the presence of p53 mutations in skin premalignant lesions suggests that these represent early events during tumor progression and additional alterations may be required for SCC development. SCC cells frequently express high levels of Np63 and Y-box binding 1 (YB-1 or YBX1) oncoproteins. Here, we show that knockdown of YB-1 in spontaneously immortalized HaCaT and non-metastatic SCC011 cells led to a dramatic decrease of Np63, cell detachment and death. In highly metastatic SCC022 cells, instead, YB-1 silencing induces PI3K/AKT signaling hyperactivation which counteracts the effect of YB-1 depletion and promotes cell survival. In summary, our results unveil a functional cross-talk between YB-1, Np63 and the PI3K/AKT pathway critically governing survival of squamous carcinoma cells. J. Cell. Physiol. 230: 2067-2074, 2015. (c) 2015 Wiley Periodicals, Inc.
机译：皮肤鳞状细胞癌(癌)通常缺乏体细胞oncogene-activating突变和他们中的大多数含有p53突变。然而,皮肤中p53突变的存在癌变前的病变表明这些代表了早期的事件在肿瘤进展和其他可能需要改变鳞状细胞癌的发展。高水平的Np63和Y-box绑定1 (YB-1或YBX1)癌基因蛋白。自发的YB-1无限增殖HaCaT和non-metastatic SCC011细胞导致了戏剧性减少Np63、细胞分离和死亡。高转移性SCC022细胞,相反,YB-1沉默诱发PI3K / AKT信号hyperactivation抵消的效果YB-1枯竭和促进细胞的生存。总结,我们的研究结果公布一项功能相声YB-1之间Np63 PI3K / AKT通路关键管理鳞状的生存癌的细胞。2067 - 2074年,2015年。

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