Cell cycle arrest is sufficient for p53-mediated tumor regression
Résumé
p53 gene therapy can induce tumor regression, but the low efficacy of in vivo gene transfer has greatly hampered the mechanistic analysis of this antitumoral activity. We therefore used a p53-null human NSCLC cell line in which we reintroduced the wild-type p53 gene under control of a tetra-cycline-dependent promoter. P53 induction provokes cell cycle arrest in G 0 /G 1 and G 2 /M phase, an up-regulation of p21, a down-regulation of cyclin B1 and appearance of sen-escence features without down-regulation of human telomer-ase reverse transcriptase. No detectable morphological