Title : TP53 alteration determines the combinational cytotoxic effect of doxorubicin and an antioxidant NAC.

Pub. Date : 2017 Jun

PMID : 28653879






4 Functional Relationships(s)
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1 In this study, doxorubicin-induced reactive oxygen species was shown to differentially affect cancer cells based on their TP53 genetic status; doxorubicin-induced apoptosis was attenuated by an antioxidant, N-acetylcysteine, in TP53 wild cells; however, N-acetylcysteine caused a synergistic increase in the apoptosis rate in TP53-altered cells. Acetylcysteine tumor protein p53 Homo sapiens
2 In this study, doxorubicin-induced reactive oxygen species was shown to differentially affect cancer cells based on their TP53 genetic status; doxorubicin-induced apoptosis was attenuated by an antioxidant, N-acetylcysteine, in TP53 wild cells; however, N-acetylcysteine caused a synergistic increase in the apoptosis rate in TP53-altered cells. Acetylcysteine tumor protein p53 Homo sapiens
3 In this study, doxorubicin-induced reactive oxygen species was shown to differentially affect cancer cells based on their TP53 genetic status; doxorubicin-induced apoptosis was attenuated by an antioxidant, N-acetylcysteine, in TP53 wild cells; however, N-acetylcysteine caused a synergistic increase in the apoptosis rate in TP53-altered cells. Acetylcysteine tumor protein p53 Homo sapiens
4 N-acetylcysteine prevented phosphorylation of P53 protein that had been induced by doxorubicin. Acetylcysteine tumor protein p53 Homo sapiens