Abstract
The role of the tumor suppressor protein p53 in apoptosis of mouse hepatoma cells was studied. Different lines were used which were either p53 wild-type or carried various types of heterozygous or homozygous p53 mutations. The presence of mutations was demonstrated to correlate with a lack in transactivating activity of p53. While UV-light effectively produced apoptosis in cells of all lines, irrespective of their p53 mutational status, γ-irradiation induced the formation of micronuclei but failed to induce apoptosis. Both UV- and γ-irradiation led to nuclear accumulation and increases in p53 protein in p53 wild-type cells. Similarly, no significant differences in apoptotic response between p53 wild-type and p53 mutated cells were seen with other apoptotic stimuli like CD95/APO-1/Fas or TNFα. These data suggest that wild-type p53 is not required for induction of apoptosis in mouse hepatoma cells which may explain the apparent lack of p53 mutations in mouse liver tumors.
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Unger, C., Buchmann, A., Bünemann, C. et al. Wild-type function of the p53 tumor suppressor protein is not required for apoptosis of mouse hepatoma cells. Cell Death Differ 5, 87–95 (1998). https://doi.org/10.1038/sj.cdd.4400321
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DOI: https://doi.org/10.1038/sj.cdd.4400321
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