Down‐regulation of Polo‐like kinase 4 (PLK4) induces G1 arrest via activation of the p38/p53/p21 signaling pathway in bladder cancer
| Autor: | Kai Wu, Ziyi Yang, Song Wu, Wenlong Ma, Guoyu Peng, Tong Ou, Haiyan Sun |
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| Rok vydání: | 2021 |
| Předmět: |
Cyclin-Dependent Kinase Inhibitor p21
Cell cycle checkpoint QH301-705.5 G1 phase arrest Polo-like kinase Protein Serine-Threonine Kinases Biology p38 Mitogen-Activated Protein Kinases General Biochemistry Genetics and Molecular Biology Metastasis Transcriptome Mice p38/p53/p21 pathway Cell Line Tumor medicine Animals Humans polo‐like kinase 4 Biology (General) Research Articles Cell growth Kinase Cancer medicine.disease G1 Phase Cell Cycle Checkpoints Gene Expression Regulation Neoplastic Urinary Bladder Neoplasms Cancer research bladder cancer Female Tumor Suppressor Protein p53 Signal transduction Research Article Signal Transduction |
| Zdroj: | FEBS Open Bio, Vol 11, Iss 9, Pp 2631-2646 (2021) FEBS Open Bio |
| ISSN: | 2211-5463 |
| Popis: | 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. We demonstrate that Polo‐like kinase 4 (PLK4) is overexpressed in human bladder cancer (BC) cell lines and tissues, and its overexpression correlates with poor prognosis. PLK4 inhibition suppresses BC cell growth and induces G1 phase arrest via activating the p38/p53/p21 pathway in vitro and in vivo. The data suggest that PLK4 might serve as a novel molecular target for BC treatment. |
| Databáze: | OpenAIRE |
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