期刊
CANCER CELL
卷 26, 期 1, 页码 61-76出版社
CELL PRESS
DOI: 10.1016/j.ccr.2014.04.030
关键词
-
资金
- Spanish Ministry of Economy and Innovation [SAF2011-28317]
- NIH [R01CA125017]
- Melanoma Research Foundation
- Spanish Ministry of Health [FIS 11/025685, FIS 11/1759]
- Fundacion Mutua Madrilena [FMM-2008-106]
- Red Tematica de Investigacion Cooperative en Cancer
- Spanish Ministry of Science and Innovation
- Fundacion La Caixa
- Fundacion Cientifica de la Asociacion Espanola Contra el Cancer
- American Cancer Society [RSG-12-076-01-LIB]
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.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据