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RNA 干扰介导的 NANOG 沉默通过 p53 信号通路导致 T 细胞急性淋巴细胞白血病细胞增殖和自我更新减少、细胞周期停滞和凋亡。

RNA interference-mediated silencing of NANOG leads to reduced proliferation and self-renewal, cell cycle arrest and apoptosis in T-cell acute lymphoblastic leukemia cells via the p53 signaling pathway.

机构信息

Department of Hematology, Nanjing Medical University, Nanjing, China.

出版信息

Leuk Res. 2013 Sep;37(9):1170-7. doi: 10.1016/j.leukres.2013.04.021. Epub 2013 May 14.

DOI:10.1016/j.leukres.2013.04.021
PMID:23683786
Abstract

NANOG is critical for maintaining the self-renewal and proliferative properties of embryonic stem cells. Here we found that cultured T-cell acute lymphoblastic leukemia (T-ALL) cells, as well as human primary T-ALL cells, express a functional variant of NANOG. NANOG mRNA is derived predominantly from a retrogene locus termed NANOGP8. Furthermore, we showed that RNA interference-mediated NANOG knockdown inhibited cell proliferation, reduced self-renewal, promoted apoptosis and arrested the cell cycle through a p53-mediated pathway in leukemic cells. These findings demonstrate the oncogenic potential of this pluripotent gene in human T-ALL cells.

摘要

NANOG 对于维持胚胎干细胞的自我更新和增殖特性至关重要。在这里,我们发现培养的 T 细胞急性淋巴细胞白血病(T-ALL)细胞以及人原发性 T-ALL 细胞表达功能性 NANOG 变体。NANOG mRNA 主要来源于称为 NANOGP8 的返座基因座。此外,我们还表明,RNA 干扰介导的 NANOG 敲低通过白血病细胞中的 p53 介导途径抑制细胞增殖,降低自我更新能力,促进细胞凋亡并使细胞周期停滞。这些发现表明该多能基因在人 T-ALL 细胞中的致癌潜力。

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