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首页> 外文期刊>Cellular Signalling >NEDD4 is overexpressed in colorectal cancer and promotes colonic cell growth independently of the PI3K/PTEN/AKT pathway
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NEDD4 is overexpressed in colorectal cancer and promotes colonic cell growth independently of the PI3K/PTEN/AKT pathway

机译：NEDD4在大肠癌中过表达，并独立于PI3K / PTEN / AKT途径促进结肠细胞生长

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摘要

Ubiquitination controls multiple cellular processes relevant to cancer pathogenesis. Using Gene Set Enrichment Analysis of an mRNA transcriptome dataset, we have identified genes encoding components of the ubiquitin system that are differentially expressed in colorectal cancers as compared to normal colonic mucosa. Among the significantly overexpressed genes was NEDD4 (neural precursor cell-expressed developmentally down-regulated 4), the prototype member of the HECT (homologous to E6AP C-terminus) E3 ubiquitin ligase family. Previous studies have shown that NEDD4 may act as an oncoprotein by inducing ubiquitination and degradation of the tumor suppressor protein PTEN (phosphatase and tensin homolog). To investigate its functional importance in colorectal cancer, HCT-15 and LoVo colon cancer cells were depleted of NEDD4 by small interfering RNA. The depletion resulted in reduced growth and altered cell morphology in both cell lines. However, NEDD4 depletion did not affect the PTEN protein level or PI3K/AKT signaling pathway activation. Moreover, ectopic expression of NEDD4 did not influence the PTEN subcellular localization or protein level. Collectively, these data demonstrate that NEDD4 is overexpressed in colorectal cancers, and suggest that NEDD4 promotes growth of colon cancer cells independently of PTEN and PI3K/AKT signaling.
机译：泛素化控制与癌症发病相关的多个细胞过程。使用mRNA转录组数据集的基因集富集分析，我们已经鉴定了与正常结肠粘膜相比在结肠直肠癌中差异表达的泛素系统组分编码基因。在明显过量表达的基因中，NEDD4（神经前体细胞表达的发育下调4）是HECT（与E6AP C端同源）E3泛素连接酶家族的原型成员。先前的研究表明，NEDD4可能通过诱导肿瘤抑制蛋白PTEN（磷酸酶和张力蛋白同源物）的泛素化和降解而起癌蛋白的作用。为了研究其在结直肠癌中的功能重要性，HCT-15和LoVo结肠癌细胞通过小干扰RNA去除了NEDD4。耗尽导致两种细胞系的生长减少和细胞形态改变。但是，NEDD4耗竭并不影响PTEN蛋白水平或PI3K / AKT信号通路的激活。此外，NEDD4的异位表达不影响PTEN亚细胞定位或蛋白质水平。总体而言，这些数据表明NEDD4在大肠癌中过表达，并暗示NEDD4可以独立于PTEN和PI3K / AKT信号传导而促进结肠癌细胞的生长。

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