Down-regulation of Polo-like kinase 4 (PLK4) induces G1 arrest via activation of the p38/p53/p21 signaling pathway in bladder cancer,FEBS Open Bio

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Down-regulation of Polo-like kinase 4 (PLK4) induces G1 arrest via activation of the p38/p53/p21 signaling pathway in bladder cancer
FEBS Open Bio ( IF 2.8 ) Pub Date : 2021-08-03 , DOI: 10.1002/2211-5463.13262
Ziyi Yang _{1,

2} , Haiyan Sun ₂ , Wenlong Ma ₂ , Kai Wu ₂ , Guoyu Peng ₂ , Tong Ou ₂ , Song Wu _{1,

2}

Affiliation

Polo-like kinase 4 (PLK4) has been reported to contribute to tumor growth, invasion, and metastasis. However, the role of PLK4 in human bladder cancer (BC) remains unclear. Here, we demonstrate the regulatory function of PLK4 in human BC progression. PLK4 is overexpressed in BC cell lines and tissues, and its overexpression correlated with poor prognosis. Our transcriptome analysis combined with subsequent functional assays indicated that PLK4 inhibition can suppress BC cell growth and induce cell cycle arrest at G1 phase via activation of the p38/p53/p21 pathway in vitro and in vivo. Overall, our data suggest that PLK4 is a critical regulator of BC cell proliferation, and thus, it may have potential as a novel molecular target for BC treatment.

中文翻译：

Polo 样激酶 4 (PLK4) 的下调通过激活膀胱癌中的 p38/p53/p21 信号通路诱导 G1 期阻滞

据报道，Polo 样激酶 4 (PLK4) 有助于肿瘤的生长、侵袭和转移。然而，PLK4 在人类膀胱癌 (BC) 中的作用仍不清楚。在这里，我们展示了 PLK4 在人类 BC 进展中的调节功能。PLK4在BC细胞系和组织中过度表达，其过度表达与不良预后相关。我们的转录组分析结合随后的功能分析表明，PLK4 抑制可以通过在体外和体内激活 p38/p53/p21 途径来抑制 BC 细胞生长并诱导细胞周期停滞在 G1 期。总体而言，我们的数据表明 PLK4 是 BC 细胞增殖的关键调节因子，因此，它可能具有作为 BC 治疗的新分子靶点的潜力。

更新日期：2021-09-01

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