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Amplification of USP13 drives ovarian cancer metabolism
Nature communications, 2016-11, Vol.7 (1), p.13525-16, Article 13525
2016

Details

Autor(en) / Beteiligte
Titel
Amplification of USP13 drives ovarian cancer metabolism
Ist Teil von
  • Nature communications, 2016-11, Vol.7 (1), p.13525-16, Article 13525
Ort / Verlag
England: Nature Publishing Group
Erscheinungsjahr
2016
Link zum Volltext
Quelle
Alma/SFX Local Collection
Beschreibungen/Notizen
  • 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.
Sprache
Englisch
Identifikatoren
ISSN: 2041-1723
eISSN: 2041-1723
DOI: 10.1038/ncomms13525
Titel-ID: cdi_doaj_primary_oai_doaj_org_article_9f59e46f1c304a21970cdebfb358fc87
Format
–
Schlagworte
1-Phosphatidylinositol 3-kinase, AKT protein, Amplification, ATP citrate lyase, Cancer, Carcinogenesis - drug effects, Carcinogenesis - genetics, Carcinogenesis - pathology, Cell Line, Tumor, Cell Proliferation - drug effects, Disease Progression, Electron transport, Endopeptidases - genetics, Endopeptidases - metabolism, Enzymes, Fatty acids, Female, Gene Amplification, Gene Knockdown Techniques, Genome, Human, Glutamine - metabolism, HEK293 Cells, Humans, Lipids - biosynthesis, Metabolism, Mitochondria, Mitochondria - drug effects, Mitochondria - metabolism, Mutation, Neoplasm Metastasis, Ovarian cancer, Ovarian carcinoma, Ovarian Neoplasms - genetics, Ovarian Neoplasms - metabolism, Ovarian Neoplasms - pathology, Peptidase, 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, Tumorigenesis, Tumors, Ubiquitin, Ubiquitin-Specific Proteases, Ubiquitination - drug effects

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