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niclosamide, cells, article, cell, fig, supplementary, google, scholar, hct, cas, figure, alox, aloxb, wildtype, tumor, cancer, singapore, data, tumors, gene, acid, mitochondrial, growth, genes, nature, mutant, response, arachidonic, pdeficient, treatment, uncoupling, human, calcium, treated, analysis, ovarian, cytochrome, drug, levels, activation, mefs, similar, mutation, measured, apoptosis, control, metabolic, significantly, compared, therapeutic,

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nature portfolio writing—review & editing privacy policy advertising univariate tools tcga rna-seq datasets nature compared wnt/beta-catenin mutant background liquid chromatography–mass spectrometry reprints italy specific research purpose nature 278 nature 358 nature 493 nature 221 nature 531 nature drug-induced proliferative arrest development genome-wide p53-binding sites p53-alox5/12b axis annexin v-fitc marker pharmakon compound library protects wild-type cells wild-type p53 evades 5-trisphosphate-induced ca2+ release including wnt/beta-catenin ms–ms spectral comparison lc–ms metabolome detection niclosamide-induced mitochondrial uncoupling wild-type p53 tumor camp-dependent protein kinase wild-type p53 lines drug free media wild-type p53 functions bona-fide p53 targets increased anti-tumorigenic effects ovarian tumor-initiating cells translating p53-based therapies wild-type p53 treated p53-dependent metabolic remodelling pre-processed data prior render tumor-specific targeting wild-type hct116 cells functional wild-type p53 wild-type p53 cells wild-type p53 tumors canonical p53-dependent genes sensitizing p53-deficient cells

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         headline:Mitochondrial uncoupling reveals a novel therapeutic opportunity for p53-defective cancers
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      headline:Mitochondrial uncoupling reveals a novel therapeutic opportunity for p53-defective cancers
      description:There are considerable challenges in directly targeting the mutant p53 protein, given the large heterogeneity of p53 mutations in the clinic. An alternative approach is to exploit the altered fitness of cells imposed by loss-of-wild-type p53. Here we identify niclosamide through a HTS screen for compounds selectively killing p53-deficient cells. Niclosamide impairs the growth of p53-deficient cells and of p53 mutant patient-derived ovarian xenografts. 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. Wild-type p53 evades the cytotoxicity by promoting the transcriptional induction of two key lipid oxygenation genes, ALOX5 and ALOX12B, which catalyzes the dioxygenation and breakdown of AA. Therefore, we propose a new paradigm for targeting cancers defective in the p53 pathway, by exploiting their vulnerability to niclosamide-induced mitochondrial uncoupling. Several challenges are involved in direct targeting of mutant p53, while targeting altered fitness of cells with loss of wild type p53 is an alternative approach. Here they identify niclosamide to be selectively toxic to p53 deficient cells through a previously unknown mitochondrial uncoupling mechanism.
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         Cancer screening
         Chemotherapy
         Drug development
         Oncology
         Science
         Humanities and Social Sciences
         multidisciplinary
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