Wild type p53 and c-myc co-operation in generating apoptosis of a rat hepatocellular carcinoma cell line (FAA-HTC1).
p53 and c-myc are both known to be involved in apoptotic cell death as well as positive or negative regulation of cell proliferation, but it is not well established whether their functions are mechanistically correlated. We found that FAA-HTC1 cells, a rat hepatocellular carcinoma cell line, expressed c-myc independently of cell cycle and no detectable p53. To investigate possible co-operation between p53 and c-myc, the dexamethasone (Dex)-inducible wild type rat p53 was stably transfected into this cell line and c-myc expression was suppressed by treatment with c-myc antisense oligonucleotide (AS). p53 expression in the p53-introduced derivative resulted in apoptotic cell death, but it did not inhibit proliferative growth of the viable cells. On the other hand, when c-myc was suppressed in the p53-expressing cells, both apoptosis and cell growth were inhibited. These results indicate that p53 can act in the same cells either as a growth-inhibitor or apoptosis-inducer depending on the status of c-myc expression.
Saito
Y
Y
Department of Pathology, Asahikawa Medical College, Japan.
Ogawa
K
K
D000818:Animals; D017209:Apoptosis; D001483:Base Sequence; D016259:Genes, myc / Q000502:physiology*; D016158:Genes, p53 / Q000502:physiology*; D008114:Liver Neoplasms, Experimental / Q000473:pathology; D008969:Molecular Sequence Data; D051381:Rats; D014407:Tumor Cells, Cultured