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
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
复制标题
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
DOI：
10.1016/j.leukres.2013.04.021
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发表时间：
2013-09-01
影响因子：
2.7
通讯作者：
Xu, Kailin
中科院分区：
文献类型：
--
作者：
Cao, Jiang;Li, Li;Xu, Kailin
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，以及人类原代T-ALL细胞，表达NANOG的功能变体。NANOG mRNA主要来源于称为NANOGP 8的逆转录基因座。此外，我们发现，RNA干扰介导的NANOG敲低抑制细胞增殖，减少自我更新，促进细胞凋亡，并通过p53介导的途径在白血病细胞中阻止细胞周期。这些发现证明了这种多能基因在人类T-ALL细胞中的致癌潜力。(C)2013爱思唯尔有限公司保留所有权利。
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. (C) 2013 Elsevier Ltd. All rights reserved.