| First Author | Happo L | Year | 2012 |
| Journal | Cell Death Dis | Volume | 3 |
| Pages | e306 | PubMed ID | 22573037 |
| Mgi Jnum | J:317500 | Mgi Id | MGI:6855039 |
| Doi | 10.1038/cddis.2012.42 | Citation | Happo L, et al. (2012) Neither loss of Bik alone, nor combined loss of Bik and Noxa, accelerate murine lymphoma development or render lymphoma cells resistant to DNA damaging drugs. Cell Death Dis 3:e306 |
| abstractText | The pro-apoptotic BH3-only protein, BIK, is widely expressed and although many critical functions in developmental or stress-induced death have been ascribed to this protein, mice lacking Bik display no overt abnormalities. It has been postulated that Bik can serve as a tumour suppressor, on the basis that its deficiency and loss of apoptotic function have been reported in many human cancers, including lymphoid malignancies. Evasion of apoptosis is a major factor contributing to c-Myc-induced tumour development, but despite this, we found that Bik deficiency did not accelerate Emu-Myc-induced lymphomagenesis. Co-operation between BIK and NOXA, another BH3-only protein, has been previously described, and was attributed to their complementary binding specificities to distinct subsets of pro-survival BCL-2 family proteins. Nevertheless, combined deficiency of Bik and Noxa did not alter the onset of Emu-Myc transgene induced lymphoma development. Moreover, although p53-mediated induction of Bik has been reported, neither Emu-Myc/Bik(-/-) nor Emu-Myc/Bik(-/-)Noxa(-/-) lymphomas were more resistant than control Emu-Myc lymphomas to killing by DNA damaging drugs, either in vitro or in vivo. These results suggest that Bik, even in combination with Noxa, is not a potent suppressor of c-Myc-driven tumourigenesis or critical for chemotherapeutic drug-induced killing of Myc-driven tumours. |
