Title : Mitochondrial uncoupling reveals a novel therapeutic opportunity for p53-defective cancers.

Pub. Date : 2018 Sep 26

PMID : 30258081






6 Functional Relationships(s)
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1 Here we identify niclosamide through a HTS screen for compounds selectively killing p53-deficient cells. Niclosamide tumor protein p53 Homo sapiens
2 Niclosamide impairs the growth of p53-deficient cells and of p53 mutant patient-derived ovarian xenografts. Niclosamide tumor protein p53 Homo sapiens
3 Niclosamide impairs the growth of p53-deficient cells and of p53 mutant patient-derived ovarian xenografts. Niclosamide tumor protein p53 Homo sapiens
4 Metabolome profiling reveals that niclosamide induces mitochondrial uncoupling, which renders mutant p53 cells susceptible to mitochondrial-dependent apoptosis through preferential accumulation of arachidonic acid (AA), and represents a first-in-class inhibitor of p53 mutant tumors. Niclosamide tumor protein p53 Homo sapiens
5 Metabolome profiling reveals that niclosamide induces mitochondrial uncoupling, which renders mutant p53 cells susceptible to mitochondrial-dependent apoptosis through preferential accumulation of arachidonic acid (AA), and represents a first-in-class inhibitor of p53 mutant tumors. Niclosamide tumor protein p53 Homo sapiens
6 Therefore, we propose a new paradigm for targeting cancers defective in the p53 pathway, by exploiting their vulnerability to niclosamide-induced mitochondrial uncoupling. Niclosamide tumor protein p53 Homo sapiens