Resistance to glucose starvation as metabolic trait of platinum-resistant human epithelial ovarian cancer cells

Oncotarget. 2017 Jan 24;8(4):6433-6445. doi: 10.18632/oncotarget.14118.

Abstract

Deregulated glucose metabolism is observed in cancer but whether this metabolic trait influences response to or is modulated by cytotoxic drugs is unknown. We show here that tumor cells from epithelial ovarian cancer (EOC) patients can be categorized, according to their in vitro viability under glucose starvation, into glucose deprivation-sensitive (glucose-addicted, GA) and glucose deprivation-resistant (glucose non-addicted, GNA). When EOC cells were cultured in the absence of glucose, all samples from platinum (PLT)-sensitive patients felt into the GA group; they disclosed higher expression of glucose metabolism enzymes, higher proliferation rates and in vitro sensitivity to PLT. Moreover, GA patients showed reduced multi-drug resistance pump expression and autophagy, compared to GNA samples. The close association between PLT sensitivity and glucose metabolic profile was confirmed in a xenograft model, where a stringent parallelism between PLT sensitivity/resistance and glucose metabolism was identified. Finally, in a cohort of naïve EOC patients categorized as GA or GNA at diagnosis, Kaplan Meier curves showed that the GA phenotype was associated with significantly better progression-free survival, compared to GNA patients.

Keywords: autophagy; glucose addiction; metabolism; ovarian cancer; platinum resistance.

Publication types

  • Comparative Study

MeSH terms

  • Aged
  • Animals
  • Antineoplastic Agents / pharmacology*
  • Carboplatin / pharmacology*
  • Carcinoma, Ovarian Epithelial
  • Cell Cycle Proteins / genetics
  • Cell Cycle Proteins / metabolism
  • Cell Line, Tumor
  • Cell Proliferation / drug effects
  • Disease-Free Survival
  • Dose-Response Relationship, Drug
  • Drug Resistance, Neoplasm*
  • Female
  • Gene Expression Regulation, Enzymologic
  • Glucose / deficiency*
  • Glycolysis / drug effects*
  • Humans
  • Kaplan-Meier Estimate
  • Mice, SCID
  • Middle Aged
  • Multidrug Resistance-Associated Proteins / genetics
  • Multidrug Resistance-Associated Proteins / metabolism
  • Neoplasms, Glandular and Epithelial / drug therapy*
  • Neoplasms, Glandular and Epithelial / genetics
  • Neoplasms, Glandular and Epithelial / metabolism
  • Neoplasms, Glandular and Epithelial / pathology
  • Ovarian Neoplasms / drug therapy*
  • Ovarian Neoplasms / genetics
  • Ovarian Neoplasms / metabolism
  • Ovarian Neoplasms / pathology
  • Phenotype
  • Time Factors
  • Xenograft Model Antitumor Assays

Substances

  • Antineoplastic Agents
  • Cell Cycle Proteins
  • Multidrug Resistance-Associated Proteins
  • Carboplatin
  • Glucose