Journal
MOLECULAR AND CELLULAR BIOLOGY
Volume 26, Issue 20, Pages 7345-7357Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/MCB.00126-06
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Funding
- NCI NIH HHS [R01 CA94989, R01 CA115638, R01 CA094989, P50 CA97257, P50 CA097257] Funding Source: Medline
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Oncogenic potential is associated with translational regulation, and the prevailing view is that oncogenes use mTOR-dependent pathways to up-regulate the synthesis of proteins critical for transformation. In this study, we show that RalA, a key mediator of Ras transformation, is also linked to the translational machinery. At least part of this linkage, however, is independent of mTOR and acts through RaIBP1 to suppress cdc42-mediated activation of S6 kinase and the translation of the antiapoptotic protein FLIP,. This action, rather than contributing to transformation, opens a latent tumor-suppressive mechanism that can be activated by tumor necrosis factor-related apoptosis -inducing ligand. These results show that the translational machinery is linked to tumor suppression as well as cell-proliferative pathways and that the reestablishment of cell death pathways by activation of the Ral oncogenic program provides a means for selective therapeutic targeting of Ral-driven malignancies.
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