Nodal activates smad and extracellular signal-regulated kinases 1/2 pathways promoting renal cell carcinoma proliferation.
Mol Med Rep
; 12(1): 587-94, 2015 Jul.
Article
en En
| MEDLINE
| ID: mdl-25672326
ABSTRACT
Expression of the nodal gene is high in a number of tumor cell types and may promote tumor growth. The expression of lefty, an inhibitor of nodal is often reduced in tumor cells. To the best of our knowledge, few studies have investigated the expression of nodal and lefty in renal cell carcinoma (RCC) cells. In the present study, quantitative polymerase chain reaction assays demonstrated that the level of nodal expression in RCC cells was high compared with that of adjacent non-tumor tissue cells, while the opposite pattern was observed for the level of lefty expression. Furthermore, lefty overexpression in RCC cells inhibited the expression of nodal. Nodal overexpression promoted RCC cell proliferation and invasion, and inhibited RCC cell apoptosis. Nodal downregulation and lefty overexpression led to similar observations The inhibition of RCC cell proliferation and invasion, and the promotion of RCC cell apoptosis. The results of the present study suggested that the expression of nodal promoted RCC growth by activating the smad and extracellular signal-regulated kinases 1/2 pathways. The expression of lefty in RCC cells was lower than that in adjacent non-tumor cells, which may result in the overexpression of nodal, thereby promoting the growth of RCC. The results of the present study may therefore be useful for the development of novel biomarkers for RCC tumor diagnosis, and suggest a potential target gene for the treatment of RCC.
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Contexto en salud:
6_ODS3_enfermedades_notrasmisibles
Problema de salud:
6_kidney_renal_pelvis_ureter_cancer
Asunto principal:
Carcinoma de Células Renales
/
Proliferación Celular
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Factores de Determinación Derecha-Izquierda
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Proteína Nodal
Límite:
Adult
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Aged
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Female
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Humans
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Male
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Middle aged
Idioma:
En
Revista:
Mol Med Rep
Año:
2015
Tipo del documento:
Article