首页> 外文期刊>The journals of gerontology.Series A. Biological sciences and medical sciences >Downregulation of polo-like kinase 1 induces cellular senescence in human primary cells through a p53-dependent pathway
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Downregulation of polo-like kinase 1 induces cellular senescence in human primary cells through a p53-dependent pathway

机译:polo样激酶1的下调通过p53依赖性途径诱导人原代细胞衰老

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Polo-like kinase 1 (PLK1) plays a key role in various stages of mitosis from entry into M phase to exit from mitosis. However, its role in cellular senescence remains to be determined. Therefore, the effects of PLK1 on cellular senescence in human primary cells were investigated. We found that expression of PLK1 decreased in human dermal fibroblasts and human umbilical vein endothelial cells under replicative senescence and premature senescence induced by adriamycin. PLK1 knockdown with PLK1 small interfering RNAs in young cells induced premature senescence. In contrast, upregulation of PLK1 in old cells partially reversed senescence phenotypes. Cellular senescence by PLK1 inhibition was observed in p16 knockdown cells but not in p53 knockdown cells. Our data suggest that PLK1 repression might result in cellular senescence in human primary cells via a p53-dependent pathway.
机译:Polo样激酶1(PLK1)在有丝分裂的各个阶段(从进入M期到退出有丝分裂)都起着关键作用。然而,其在细胞衰老中的作用尚待确定。因此,研究了PLK1对人原代细胞衰老的影响。我们发现在阿霉素诱导的复制性衰老和过早衰老下,人皮肤成纤维细胞和人脐静脉内皮细胞中PLK1的表达下降。在年轻细胞中用PLK1小干扰RNA击倒PLK1会导致早衰。相反,旧细胞中PLK1的上调部分逆转了衰老表型。在p16击倒细胞中观察到PLK1抑制引起的细胞衰老,而在p53击倒细胞中未观察到。我们的数据表明,PLK1抑制可能通过p53依赖性途径导致人原代细胞衰老。

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