| First Author | Kashatus D | Year | 2006 |
| Journal | Genes Dev | Volume | 20 |
| Issue | 2 | Pages | 225-35 |
| PubMed ID | 16384933 | Mgi Jnum | J:104618 |
| Mgi Id | MGI:3612375 | Doi | 10.1101/gad.1352206 |
| Citation | Kashatus D, et al. (2006) Expression of the Bcl-3 proto-oncogene suppresses p53 activation. Genes Dev 20(2):225-35 |
| abstractText | While Bcl-3 expression in cancer was originally thought to be limited to B-cell lymphomas with a 14;19 chromosomal translocation, more recent evidence indicates that expression of this presumptive oncoprotein is significantly more widespread in cancer. However, an oncogenic role for Bcl-3 has not been clearly identified. Experiments presented here indicate that Bcl-3 is inducible by DNA damage and is required for the induction of Hdm2 gene expression and the suppression of persistent p53 activity. Furthermore, constitutive expression of Bcl-3 suppresses DNA damage-induced p53 activation and inhibits p53-induced apoptosis through a mechanism that is at least partly dependent on the up-regulation of Hdm2. The results provide insight into a mechanism whereby altered expression of Bcl-3 leads to tumorigenic potential. Since Bcl-3 is required for germinal center formation, these results suggest functional similarities with the unrelated Bcl-6 oncoprotein in suppressing potential p53-dependent cell cycle arrest and apoptosis in response to somatic hypermutation and class switch recombination. |
