Journal article
Bax suppresses tumorigenesis and stimulates apoptosis in vivo
Nature (London), Vol.385(6617), pp.637-640
02/1997
DOI: 10.1038/385637a0
PMID: 9024662
Abstract
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.
Details
- Title: Subtitle
- Bax suppresses tumorigenesis and stimulates apoptosis in vivo
- Creators
- Chaoying YinC. Michael KnudsonStanley J KorsmeyerTerry Van Dyke
- Resource Type
- Journal article
- Publication Details
- Nature (London), Vol.385(6617), pp.637-640
- DOI
- 10.1038/385637a0
- PMID
- 9024662
- ISSN
- 0028-0836
- eISSN
- 1476-4687
- Language
- English
- Date published
- 02/1997
- Academic Unit
- Pathology; Radiation Oncology
- Record Identifier
- 9984047698402771
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