Bax suppresses tumorigenesis and stimulates apoptosis in vivo

Chaoying Yin, C. Michael Knudson, Stanley J. Korsmeyer and Terry Van Dyke
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Chaoying Yin: University of North Carolina School of Medicine at Chapel Hill
C. Michael Knudson: Washington University School of Medicine
Stanley J. Korsmeyer: Washington University School of Medicine
Terry Van Dyke: University of North Carolina School of Medicine at Chapel Hill

Nature, 1997, vol. 385, issue 6617, 637-640

Abstract: 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 cent1. 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.

Date: 1997
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DOI: 10.1038/385637a0

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