期刊
CANCER CELL
卷 16, 期 2, 页码 149-160出版社
CELL PRESS
DOI: 10.1016/j.ccr.2009.06.008
关键词
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资金
- European Commission [LSH-CT-2003-506803]
- Austrian Research Fund [P19530-B11]
- Austrian Science Fund (FWF) [P19530] Funding Source: Austrian Science Fund (FWF)
Ras activation is common to many human cancers and promotes cell proliferation and survival by initiating multiple signaling cascades. Accordingly, Ras-transformed cells are generally considered too resourceful to become addicted to a single effector. In contrast to this tenet, we now demonstrate an absolute, cell autonomous requirement for Raf-1 in the development and maintenance of Ras-induced skin epidermis tumors. Mechanistically, Raf-1 functions as an endogenous inhibitor dimming the activity of the Rho-dependent kinase Rok-alpha in the context of a Ras-induced Raf-1:Rok-a complex. Raf-1-induced Rok-alpha inhibition allows the phosphorylation of STAT3 and Myc expression and promotes dedifferentiation in Ras-induced tumors. These data link the Raf-1:Rok-alpha complex to STAT3/Myc activation and delineate a pathway crucial for cell fate decision in Ras-induced tumorigenesis.
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