Targeting Glutamine Utilization in Therapy-Resistant Prostate Cancer

Abstract

Advanced and aggressive prostate cancer (PCa) depend on glutamine for tumor survival and proliferation. We have previously shown that inhibition of glutaminase 1, which catalyzes the rate-limiting step of glutamine catabolism, achieves significant therapeutic effect; however, therapy resistance is inevitable. Here we report that while the glutamine carbon is critical to PCa survival, a parallel pathway of glutamine nitrogen catabolism that actively contributes to pyrimidine assembly is equally important for PCa cells. Importantly, we demonstrate a reciprocal feedback mechanism between glutamine carbon and nitrogen pathways which leads to therapy resistance when one of the two pathways is inhibited. Combination treatment to inhibit both pathways simultaneously yields better clinical outcome for advanced PCa patients.

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Document Details

Document Type
Technical Report
Publication Date
Mar 01, 2023
Accession Number
AD1203896

Entities

People

  • Jiaoti Huang
  • Xue Jiang

Organizations

  • Duke University

Tags

DTIC Thesaurus Topics

  • Biomedical Information Systems
  • Biomedical Research
  • Cell Line
  • Chemistry
  • Computational Biology
  • Culture Techniques
  • Electronic Mail
  • Gene Expression
  • Genes
  • Glutamates
  • Inhibition
  • Metabolic Pathways
  • Metabolism
  • Metabolomics
  • Neoplasms
  • Nucleotides
  • Prostate Cancer
  • Proteins
  • Resistance
  • Tissues

Fields of Study

  • Biology

Readers

  • Prostate Cancer Biology.