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
; 11(9): 2631-2646, 2021 09.
Article
em En
| MEDLINE
| ID: mdl-34342940
ABSTRACT
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.
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Texto completo:
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Base de dados:
MEDLINE
Assunto principal:
Neoplasias da Bexiga Urinária
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Proteína Supressora de Tumor p53
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Proteínas Serina-Treonina Quinases
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Proteínas Quinases p38 Ativadas por Mitógeno
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Inibidor de Quinase Dependente de Ciclina p21
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Pontos de Checagem da Fase G1 do Ciclo Celular
Limite:
Animals
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Female
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Humans
Idioma:
En
Ano de publicação:
2021
Tipo de documento:
Article