| First Author | Oeckinghaus A | Year | 2014 |
| Journal | Cell Rep | Volume | 8 |
| Issue | 6 | Pages | 1793-1807 |
| PubMed ID | 25220458 | Mgi Jnum | J:277582 |
| Mgi Id | MGI:6274062 | Doi | 10.1016/j.celrep.2014.08.015 |
| Citation | Oeckinghaus A, et al. (2014) kappaB-Ras proteins regulate both NF-kappaB-dependent inflammation and Ral-dependent proliferation. Cell Rep 8(6):1793-1807 |
| abstractText | The transformation of cells generally involves multiple genetic lesions that undermine control of both cell death and proliferation. We now report that kappaB-Ras proteins act as regulators of NF-kappaB and Ral pathways, which control inflammation/cell death and proliferation, respectively. Cells lacking kappaB-Ras therefore not only show increased NF-kappaB activity, which results in increased expression of inflammatory mediators, but also exhibit elevated Ral activity, which leads to enhanced anchorage-independent proliferation (AIP). kappaB-Ras deficiency consequently leads to significantly increased tumor growth that can be dampened by inhibiting either Ral or NF-kappaB pathways, revealing the unique tumor-suppressive potential of kappaB-Ras proteins. Remarkably, numerous human tumors show reduced levels of kappaB-Ras, and increasing the level of kappaB-Ras in these tumor cells impairs their ability to undergo AIP, thereby implicating kappaB-Ras proteins in human disease. |
