p38gamma overexpression promotes renal cell carcinoma cell growth, proliferation and migration.
Biochem Biophys Res Commun
; 516(2): 466-473, 2019 08 20.
Article
en En
| MEDLINE
| ID: mdl-31229268
Recent studies have proposed that p38gamma (p38γ) might be critically involved in tumorigenesis and cancer progression. Its expression and potential functions in human renal cell carcinoma (RCC) are studied here. We show that p38γ mRNA and protein levels are upregulated in human RCC tissues, as compared to its levels in the surrounding normal renal tissues. p38γ upregulation was also detected in established (786-O line) and primary human RCC cells. Functional studies in 786-O cells and primary human RCC cells demonstrated that p38γ silencing (by targeted shRNAs) or CRISPR/Cas9-mediated p38γ knockout (KO) potently inhibited cell growth, viability, proliferation and migration. Furthermore, p38γ shRNA or KO in RCC cells decreased retinoblastoma (Rb) phosphorylation and downregulated cyclin E1/A expression. Additionally, significant apoptosis activation was detected in p38γ-silenced and p38γ-KO RCC cells. Contrarily, ectopic overexpression of p38γ facilitated cell growth, viability, proliferation and migration in RCC cells. Taken together, we show that p38γ overexpression promotes RCC cell growth, proliferation and migration. p38γ could be a novel therapeutic target for human RCC.
Palabras clave
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Carcinoma de Células Renales
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Movimiento Celular
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Proteína Quinasa 12 Activada por Mitógenos
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Neoplasias Renales
Límite:
Adult
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Aged
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Humans
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Male
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Middle aged
Idioma:
En
Revista:
Biochem Biophys Res Commun
Año:
2019
Tipo del documento:
Article
País de afiliación:
China
Pais de publicación:
Estados Unidos