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Targeting pyrimidine synthesis accentuates molecular therapy response in glioblastoma stem cells
Journal article   Peer reviewed

Targeting pyrimidine synthesis accentuates molecular therapy response in glioblastoma stem cells

Xiuxing Wang, Kailin Yang, Qiulian Wu, Leo J. Y. Kim, Andrew R. Morton, Ryan C. Gimple, Briana C. Prager, Yu Shi, Wenchao Zhou, Shruti Bhargava, …
Science translational medicine, Vol.11(504), 4972
08/07/2019
DOI: 10.1126/scitranslmed.aau4972
PMCID: PMC7568232
PMID: 31391321
url
https://www.ncbi.nlm.nih.gov/pmc/articles/7568232View
Open Access

Abstract

Glioblastoma stem cells (GSCs) reprogram glucose metabolism by hijacking high-affinity glucose uptake to survive in a nutritionally dynamic microenvironment. Here, we trace metabolic aberrations in GSCs to link core genetic mutations in glioblastoma to dependency on de novo pyrimidine synthesis. Targeting the pyrimidine synthetic rate-limiting step enzyme carbamoyl-phosphate synthetase 2, aspartate transcarbamylase, dihydroorotase (CAD) or the critical downstream enzyme dihydroorotate dehydrogenase (DHODH) inhibited GSC survival, self-renewal, and in vivo tumor initiation through the depletion of the pyrimidine nucleotide supply in rodent models. Mutations in EGFR or PTEN generated distinct CAD phosphorylation patterns to activate carbon influx through pyrimidine synthesis. Simultaneous abrogation of tumor-specific driver mutations and DHODH activity with clinically approved inhibitors demonstrated sustained inhibition of metabolic activity of pyrimidine synthesis and GSC tumorigenic capacity in vitro. Higher expression of pyrimidine synthesis genes portends poor prognosis of patients with glioblastoma. Collectively, our results demonstrate a therapeutic approach of precision medicine through targeting the nexus between driver mutations and metabolic reprogramming in cancer stem cells.
Cell Biology Life Sciences & Biomedicine Medicine, Research & Experimental Research & Experimental Medicine Science & Technology

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