Title : Transcription-independent and -dependent p53-mediated apoptosis in response to genotoxic and non-genotoxic stress.

Pub. Date : 2019

PMID : 31482012






6 Functional Relationships(s)
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1 In addition to doxorubicin, our results here indicated that camptothecin and bortezomib, which are a topoisomerase 1 poison and a 26 S proteasome inhibitor, respectively, could also induce apoptosis in a p53-dependent manner in prostate cancer. Camptothecin tumor protein p53 Homo sapiens
2 By using dominant negative p53 to compete with wild-type p53 in transcription activity, we demonstrated that p53-mediated apoptosis in response to doxorubicin- or camptothecin-induced genotoxic stress is transcription-independent. Camptothecin tumor protein p53 Homo sapiens
3 By using dominant negative p53 to compete with wild-type p53 in transcription activity, we demonstrated that p53-mediated apoptosis in response to doxorubicin- or camptothecin-induced genotoxic stress is transcription-independent. Camptothecin tumor protein p53 Homo sapiens
4 By using dominant negative p53 to compete with wild-type p53 in transcription activity, we demonstrated that p53-mediated apoptosis in response to doxorubicin- or camptothecin-induced genotoxic stress is transcription-independent. Camptothecin tumor protein p53 Homo sapiens
5 Interestingly, we also found that doxorubicin-induced p21 expression is activated by p53 in transcription-dependent manner, while camptothecin-induced p21 expression is p53-independent. Camptothecin tumor protein p53 Homo sapiens
6 We then investigated the p53 ratio of nucleus to cytosol corresponding to low and high dose doxorubicin, camptothecin, or bortezomib treatment. Camptothecin tumor protein p53 Homo sapiens