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TY - JOUR AU - Yin, Chaoying AU - Knudson, C. Michael AU - Korsmeyer, Stanley J. AU - Dyke, Terry Van PY - 1997 DA - 1997/02/01 TI - Bax suppresses tumorigenesis and stimulates apoptosis in vivo JO - Nature SP - 637 EP - 640 VL - 385 IS - 6617 AB - 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. SN - 1476-4687 UR - https://doi.org/10.1038/385637a0 DO - 10.1038/385637a0 ID - Yin1997 ER -