κB-Ras proteins regulate both NF-κB-dependent inflammation and Ral-dependent proliferation.

ABSTRACT: The transformation of cells generally involves multiple genetic lesions that undermine control of both cell death and proliferation. We now report that κB-Ras proteins act as regulators of NF-κB and Ral pathways, which control inflammation/cell death and proliferation, respectively. Cells lacking κB-Ras therefore not only show increased NF-κB activity, which results in increased expression of inflammatory mediators, but also exhibit elevated Ral activity, which leads to enhanced anchorage-independent proliferation (AIP). κB-Ras deficiency consequently leads to significantly increased tumor growth that can be dampened by inhibiting either Ral or NF-κB pathways, revealing the unique tumor-suppressive potential of κB-Ras proteins. Remarkably, numerous human tumors show reduced levels of κB-Ra

SUBMITTER: Oeckinghaus A 

PROVIDER: S-EPMC4177457 | biostudies-literature | 2014 Sep

REPOSITORIES: biostudies-literature