53 tumour suppressor is ubiquitously expressed in the early stages of mammalian embryogenesis. There is evidence of its involvement in the control of early development and differentiation, however, the molecular mechanisms of its action during embryogenesis are unknown. The role of p53 in the response to stress, which causes its accumulation and/or activation, is better understood. There are two alternative cellular responses to p53 activation : either arrest of the cell cycle or induction of programmed cell death (apoptosis). Both responses give rise to the phenotype of tumour growth suppression. Loss of p53 activity, frequently observed during tumorigenesis, allows survival and proliferation of cells which would otherwise be eliminated.
In this review, we briefly describe the current state of knowledge of the molecular mechanisms participating in the different biological functions of p53. We then discuss in more detail the double role the p53 seems to play in the control of apoptosis.