Department of Radiation Oncology, Emory University School of Medicine, Winship Cancer Institute of Emory University, Atlanta, GA, USA.
Division of Space Life Sciences, Universities Space Research Association, Houston, TX, USA.
Cell Death Dis. 2014 Jan 23;5(1):e1024. doi: 10.1038/cddis.2013.563.
Human cell transformation is a key step for oncogenic development, which involves multiple pathways; however, the mechanism remains unclear. To test our hypothesis whether cell oncogenic transformation shares some mechanisms with the process of reprogramming non-stem cells to induced pluripotent stem cells (iPSC), we studied the relationship among the key factors for promoting or inhibiting iPSC in radiation-transformed human epithelial cell lines derived from different tissues (lung, breast and colon). We unexpectedly found that p63 and OCT4 were highly expressed (accompanied by low expressed p53 and miR-34a) in all transformed cell lines examined when compared with their non-transformed counterparts. We further elucidated the relationship of these factors: the 3p strand of miR-34a directly targeted OCT4 by binding to the 3' untranslated region (3'-UTR) of OCT4 and, OCT4, in turn, stimulated p63 but inhibited p53 expression by binding to a specific region of the p63 or p53 promoter. Moreover, we revealed that the effects of OCT4 on promoting cell oncogenic transformation were by affecting p63 and p53. These results support that a positive loop exists in human cells: OCT4 upregulation as a consequence of inhibition of miR-34a, promotes p63 but suppresses p53 expression, which further stimulates OCT4 upregulation by downregulating miR-34a. This functional loop contributes significantly to cell transformation and, most likely, also to the iPSC process.
人类细胞转化是致癌发展的关键步骤,涉及多个途径;然而,其机制尚不清楚。为了验证我们的假设,即细胞致癌转化是否与将非干细胞重编程为诱导多能干细胞(iPSC)的过程共享一些机制,我们研究了促进或抑制源自不同组织(肺、乳腺和结肠)的辐射转化人上皮细胞系中 iPSC 的关键因素之间的关系。我们出人意料地发现,与未转化的细胞相比,所有转化细胞系中 p63 和 OCT4 的表达水平均升高(同时伴有低表达的 p53 和 miR-34a)。我们进一步阐明了这些因素之间的关系:miR-34a 的 3p 链通过与 OCT4 的 3'非翻译区(3'-UTR)结合而直接靶向 OCT4,而 OCT4 则通过结合 p63 或 p53 启动子的特定区域来刺激 p63 但抑制 p53 表达。此外,我们揭示了 OCT4 对促进细胞致癌转化的影响是通过影响 p63 和 p53 实现的。这些结果支持人细胞中存在正反馈环:miR-34a 抑制的结果是 OCT4 的上调,促进了 p63 的表达,但抑制了 p53 的表达,这进一步通过下调 miR-34a 来刺激 OCT4 的上调。这个功能环对细胞转化有重要贡献,很可能对 iPSC 过程也有重要贡献。
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