RAB7 controls melanoma progression by exploiting a lineage-specific wiring of the endolysosomal pathway. [artículo]
Por: Ortiz Romero, Pablo Luis [Dermatología Médico-Quirúrgica y Venereología]
| Rodríguez Peralto, José Luis [Anatomía Patológica].
Colaborador(es): Servicio de Dermatología Médico-Quirúrgica y Venereología | Instituto de Investigación imas12 | Servicio de Anatomía Patológica.
Tipo de material: 
ArtículoEditor: Cancer cell, 2014Descripción: 26(1):61-76.Recursos en línea: Solicitar documento Resumen: Although common cancer hallmarks are well established, lineage-restricted oncogenes remain less understood. Here, we report an inherent dependency of melanoma cells on the small GTPase RAB7, identified within a lysosomal gene cluster that distinguishes this malignancy from over 35 tumor types. Analyses in human cells, clinical specimens, and mouse models demonstrated that RAB7 is an early-induced melanoma driver whose levels can be tuned to favor tumor invasion, ultimately defining metastatic risk. Importantly, RAB7 levels and function were independent of MITF, the best-characterized melanocyte lineage-specific transcription factor. Instead, we describe the neuroectodermal master modulator SOX10 and the oncogene MYC as RAB7 regulators. These results reveal a unique wiring of the lysosomal pathway that melanomas exploit to foster tumor progression.
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Artículo
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PC16566 (Navegar estantería) | Disponible |
Formato Vancouver:
Alonso Curbelo D, Riveiro Falkenbach E, Pérez Guijarro E, Cifdaloz M, Karras P, Osterloh L et al. RAB7 controls melanoma progression by exploiting a lineage-specific wiring of the endolysosomal pathway. Cancer Cell. 2014 Jul 14;26(1):61-76.
PMID: 24981740
Contiene 51 referencias
Although common cancer hallmarks are well established, lineage-restricted oncogenes remain less understood. Here, we report an inherent dependency of melanoma cells on the small GTPase RAB7, identified within a lysosomal gene cluster that distinguishes this malignancy from over 35 tumor types. Analyses in human cells, clinical specimens, and mouse models demonstrated that RAB7 is an early-induced melanoma driver whose levels can be tuned to favor tumor invasion, ultimately defining metastatic risk. Importantly, RAB7 levels and function were independent of MITF, the best-characterized melanocyte lineage-specific transcription factor. Instead, we describe the neuroectodermal master modulator SOX10 and the oncogene MYC as RAB7 regulators. These results reveal a unique wiring of the lysosomal pathway that melanomas exploit to foster tumor progression.
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