| First Author | Yin C | Year | 1997 |
| Journal | Nature | Volume | 385 |
| Issue | 6617 | Pages | 637-40 |
| PubMed ID | 9024662 | Mgi Jnum | J:38331 |
| Mgi Id | MGI:85706 | Doi | 10.1038/385637a0 |
| Citation | Yin C, et al. (1997) Bax suppresses tumorigenesis and stimulates apoptosis in vivo. Nature 385(6617):637-40 |
| abstractText | The protein p53 is a key tumour-suppressor, as evidenced by its frequent inactivation in human cancers. Animal models have indicated that attenuation of p53-dependent cell death (apoptosis) can contribute to both the initiation and progression of cancer, but the molecular mechanisms are unknown. Although p53-mediated transcriptional activation is one possible explanation, none of the known p53-responsive genes has been shown to function in p53-dependent apoptosis. Here we test the role of the death-promoting gene bax in a transgenic mouse brain tumour, a model in which p53-mediated apoptosis attenuates tumour growth. Inactivation of p53 causes a dramatic acceleration of tumour growth owing to a reduction in apoptosis of over ninety per cent. We show that p53-dependent expression of bax is induced in slow-growing apoptotic tumours. Moreover, tumour growth is accelerated and apoptosis drops by fifty per cent in Bax-deficient mice, indicating that it is required for a full p53-mediated response. To our knowledge this is the first demonstration that Bax acts as a tumour suppressor, and our findings indicate that Bax could be a component of the p53-mediated apoptotic response in this system. |
