作者: Chaoying Yin , C. Michael Knudson , Stanley J. Korsmeyer , Terry Van Dyke
DOI: 10.1038/385637A0
关键词: Cancer research 、 Apoptosis 、 Bcl-2-associated X protein 、 Regulation of gene expression 、 Molecular biology 、 Tumor suppressor gene 、 Carcinogenesis 、 Genetically modified mouse 、 Transgene 、 Biology 、 Programmed cell death
摘要: 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 cancer, but molecular mechanisms are unknown. Although p53-mediated transcriptional activation one possible explanation, none known p53-responsive genes has been shown function apoptosis. Here we test role death-promoting gene bax transgenic mouse brain tumour, model which apoptosis attenuates tumour growth. Inactivation causes dramatic acceleration growth owing reduction over ninety per cent. We show expression induced slow-growing apoptotic tumours. Moreover, accelerated drops fifty cent Bax-deficient mice, indicating it required for full response. To our knowledge this first demonstration Bax acts suppressor, findings indicate could be component response system.