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• W2973160589 abstract "Abstract Treatment of cancer with poly (ADP-ribose) polymerase (PARP) inhibitors is currently limited to cells defective in the homologous recombination (HR) pathway. Identification of genetic targets that induce or mimic HR deficiencies will extend the clinical utility of PARP inhibitors. Here we perform a CRISPR/Cas9-based genome-scale loss-of-function screen, using the sensitivity of PARP inhibitor olaparib as a surrogate. We identify C12orf5 , encoding TP53 induced glycolysis and apoptosis regulator (TIGAR), as a modifier of PARP inhibitor response. We show that TIGAR is amplified in several cancer types, and higher expression of TIGAR associates with poor overall survival in ovarian cancer. TIGAR knockdown enhances sensitivity to olaparib in cancer cells via downregulation of BRCA1 and the Fanconi anemia pathway and increases senescence of these cells by affecting metabolic pathways and increasing the cytotoxic effects of olaparib. Our results indicate TIGAR should be explored as a therapeutic target for treating cancer and extending the use of PARP inhibitors." @default.
• W2973160589 created "2019-09-19" @default.
• W2973160589 creator A5001092701 @default.
• W2973160589 creator A5036737144 @default.
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• W2973160589 date "2019-09-09" @default.
• W2973160589 modified "2023-10-16" @default.
• W2973160589 title "Genome-scale CRISPR knockout screen identifies TIGAR as a modifier of PARP inhibitor sensitivity" @default.
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• W2973160589 doi "https://doi.org/10.1038/s42003-019-0580-6" @default.
• W2973160589 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6733792" @default.
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• W2973160589 hasPublicationYear "2019" @default.
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