NOTCH pathway inactivation promotes bladder cancer progression. [artículo]
Por: Dueñas, Marta [Instituto de Investigación i+12]
| Martínez Fernández, Mónica [Instituto de Investigación i+12] | Paramio, Jesús M [Instituto de Investigación i+12].
Colaborador(es): Instituto de Investigación imas12.
Tipo de material: 
ArtículoEditor: The Journal of clinical investigation, 2015Descripción: 125(2):824-30.Recursos en línea: Acceso libre Resumen: NOTCH signaling suppresses tumor growth and proliferation in several types of stratified epithelia. Here, we show that missense mutations in NOTCH1 and NOTCH2 found in human bladder cancers result in loss of function. In murine models, genetic ablation of the NOTCH pathway accelerated bladder tumorigenesis and promoted the formation of squamous cell carcinomas, with areas of mesenchymal features. Using bladder cancer cells, we determined that the NOTCH pathway stabilizes the epithelial phenotype through its effector HES1 and, consequently, loss of NOTCH activity favors the process of epithelial-mesenchymal transition. Evaluation of human bladder cancer samples revealed that tumors with low levels of HES1 present mesenchymal features and are more aggressive. Together, our results indicate that NOTCH serves as a tumor suppressor in the bladder and that loss of this pathway promotes mesenchymal and invasive features.
| Tipo de ítem | Ubicación actual | Signatura | Estado | Fecha de vencimiento |
|---|---|---|---|---|
Artículo
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PC17190 (Navegar estantería) | Disponible |
Navegando Hospital Universitario 12 de Octubre Estantes Cerrar el navegador de estanterías
Formato Vancouver:
Maraver A, Fernández Marcos PJ, Cash TP, Méndez Pertuz M, Dueñas M, Maietta P et al. NOTCH pathway inactivation promotes bladder cancer progression. J Clin Invest. 2015 Feb;125(2):824-30.
PMID: 25574842
PMC4319408
Contiene 51 referencias
NOTCH signaling suppresses tumor growth and proliferation in several types of stratified epithelia. Here, we show that missense mutations in NOTCH1 and NOTCH2 found in human bladder cancers result in loss of function. In murine models, genetic ablation of the NOTCH pathway accelerated bladder tumorigenesis and promoted the formation of squamous cell carcinomas, with areas of mesenchymal features. Using bladder cancer cells, we determined that the NOTCH pathway stabilizes the epithelial phenotype through its effector HES1 and, consequently, loss of NOTCH activity favors the process of epithelial-mesenchymal transition. Evaluation of human bladder cancer samples revealed that tumors with low levels of HES1 present mesenchymal features and are more aggressive. Together, our results indicate that NOTCH serves as a tumor suppressor in the bladder and that loss of this pathway promotes mesenchymal and invasive features.
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