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Mutant p53 Enhances Nuclear Factor B Activation by Tumor Necrosis Factor in Cancer Cells

¹ Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel; ² Department of Experimental Oncology, Regina Elena Cancer Institute, ³ Rome Oncogenomic Center, Via delle Messi d'oro and ⁴ Fondazione Andrea Cesalpino, University La Sapienza, Rome, Italy; and ⁵ Molecular Carcinogenesis Group, Department of Histology and Embryology, School of Medicine, University of Athens, Greece

Requests for reprints: Moshe Oren, Molecular Cell Biology, Weizmann Institute, Rehovot 76100, Israel. Phone: 972-8-9342358; Fax: 972-8-9346004; E-mail: moshe.oren{at}weizmann.ac.il.

Mutations in the p53 tumor suppressor are very frequent in human cancer. Often, such mutations lead to the constitutive overproduction of mutant p53 proteins, which may exert a cancer-promoting gain of function. We now report that cancer-associated mutant p53 can augment the induction of nuclear factor B (NFB) transcriptional activity in response to the cytokine tumor necrosis factor (TNF). Conversely, down-regulation of endogenous mutant p53 sensitizes cancer cells to the apoptotic effects of TNF. Analysis of human head and neck tumors and lung tumors reveals a close correlation between the presence of abundant mutant p53 proteins and the constitutive activation of NFB. Together, these findings suggest that p53 mutations may promote cancer progression by augmenting NFB activation in the context of chronic inflammation. [Cancer Res 2007;67(6):2396–401]

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