| First Author | Ehrenreiter K | Year | 2009 |
| Journal | Cancer Cell | Volume | 16 |
| Issue | 2 | Pages | 149-60 |
| PubMed ID | 19647225 | Mgi Jnum | J:151973 |
| Mgi Id | MGI:4355643 | Doi | 10.1016/j.ccr.2009.06.008 |
| Citation | Ehrenreiter K, et al. (2009) Raf-1 addiction in Ras-induced skin carcinogenesis. Cancer Cell 16(2):149-60 |
| abstractText | 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-alpha 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. |
