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Poly(ADP-ribose) glycohydrolase inhibition sequesters NAD+ to potentiate the metabolic lethality of alkylating chemotherapy in IDH mutant tumor cells

Cancer Discov. 2020; 
Hiroaki Nagashima, Christine K Lee, Kensuke Tateishi, Fumi Higuchi, Megha Subramanian, Seamus Rafferty, Lisa Melamed, Julie J Miller, Hiroaki Wakimoto, Daniel P Cahill
Products/Services Used Details Operation
ORF cDNA Clones/MolecularCloud … PARP1 cDNA ORF clone (Cat #: OHu2551) and control vector (pcDNA3.1+/C- (K)DYK, Cat # SC1849) were purchased from GenScript. Transfection was carried out using Opti … gRNA from Genscript (gRNA2 and 3). Non-targeting gRNA lentivirus vector was from Genscript Get A Quote

摘要

Nicotinamide adenine dinucleotide (NAD+) is an essential cofactor metabolite and is the currency of metabolic transactions critical for cell survival. Depending on tissue context and genotype, cancer cells have unique dependencies on NAD+ metabolic pathways. Poly(ADP-ribose) polymerases (PARPs) catalyze oligomerization of NAD+ monomers into poly(ADP-ribose) (PAR) chains during cellular response to alkylating chemotherapeutics, including procarbazine or temozolomide. Here, we find that, in endogenous IDH1 mutant tumor models, alkylator-induced cytotoxicity is markedly augmented by pharmacologic inhibition or genetic knockout of the PAR breakdown enzyme poly(ADP-ribose) glycohydrolase (PARG). Both in vitro and in... More

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