Amplification of USP13 drives ovarian cancer metabolism

Nat Commun. 2016 Nov 28:7:13525. doi: 10.1038/ncomms13525.

Abstract

Dysregulated energetic metabolism has been recently identified as a hallmark of cancer. Although mutations in metabolic enzymes hardwire metabolism to tumourigenesis, they are relatively infrequent in ovarian cancer. More often, cancer metabolism is re-engineered by altered abundance and activity of the metabolic enzymes. Here we identify ubiquitin-specific peptidase 13 (USP13) as a master regulator that drives ovarian cancer metabolism. USP13 specifically deubiquitinates and thus upregulates ATP citrate lyase and oxoglutarate dehydrogenase, two key enzymes that determine mitochondrial respiration, glutaminolysis and fatty acid synthesis. The USP13 gene is co-amplified with PIK3CA in 29.3% of high-grade serous ovarian cancers and its overexpression is significantly associated with poor clinical outcome. Inhibiting USP13 remarkably suppresses ovarian tumour progression and sensitizes tumour cells to the treatment of PI3K/AKT inhibitor. Our results reveal an important metabolism-centric role of USP13, which may lead to potential therapeutics targeting USP13 in ovarian cancers.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Carcinogenesis / drug effects
  • Carcinogenesis / genetics
  • Carcinogenesis / pathology
  • Cell Line, Tumor
  • Cell Proliferation / drug effects
  • Disease Progression
  • Endopeptidases / genetics*
  • Endopeptidases / metabolism
  • Female
  • Gene Amplification*
  • Gene Knockdown Techniques
  • Genome, Human
  • Glutamine / metabolism
  • HEK293 Cells
  • Humans
  • Lipids / biosynthesis
  • Mitochondria / drug effects
  • Mitochondria / metabolism
  • Neoplasm Metastasis
  • Ovarian Neoplasms / genetics*
  • Ovarian Neoplasms / metabolism*
  • Ovarian Neoplasms / pathology
  • Protein Kinase Inhibitors / pharmacology
  • Protein Stability / drug effects
  • Proto-Oncogene Proteins c-akt / antagonists & inhibitors
  • Proto-Oncogene Proteins c-akt / metabolism
  • Substrate Specificity / drug effects
  • Ubiquitin-Specific Proteases
  • Ubiquitination / drug effects

Substances

  • Lipids
  • Protein Kinase Inhibitors
  • Glutamine
  • Proto-Oncogene Proteins c-akt
  • Endopeptidases
  • USP13 protein, human
  • Ubiquitin-Specific Proteases