Mutations affecting the p53 gene abrogate its tumor suppressor activity. It is, however, unclear whether such mutations can generate mutant p53 proteins with an intrinsic transforming ability. More importantly, the mechanism(s) by which they exert such activity is unknown. We report here that p53-deficient hepatoma cells (Hep3B) transfected with mutant p53-249ser (codon 249 Arg→Ser) acquire a new phenotype with an increased in vitro survival and mitotic activity. However, such a phenotypic change is not sufficient to cause a major shift in the poor tumorigenic potential of these cells. This is apparently due to transforming growth factor β1-mediated apoptotic death of Hep3B cells which is not affected by the expression of p53-249ser.


This work was supported by grants from Comité Départemental de l'Ain de La Ligue de Lutte Contre le Cancer, and the NIH (CA-54567). F. P. was supported by fellowships from the Institut de Formation Superieure Biomedicale and La Ligue National de Lutte Contre le Cancer.

This content is only available via PDF.