Nature communications · 2016
Amplification of USP13 drives ovarian cancer metabolism.
СтатьяПоддержка NIH: внешняя программаПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Han Cecil, Yang Lifeng, Choi Hyun Ho, Baddour Joelle, Achreja Abhinav, Liu Yunhua, Li Yujing, Li Jiada, Wan Guohui, Huang Cheng, Ji Guang, Zhang Xinna, Nagrath Deepak, Lu Xiongbin
Аннотация
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.
Предметные рубрики MeSH
CarcinogenesisCell Line, TumorCell ProliferationDisease ProgressionEndopeptidasesFemaleGene AmplificationGene Knockdown TechniquesGenome, HumanGlutamineHEK293 CellsHumansLipidsMitochondriaNeoplasm MetastasisOvarian NeoplasmsProtein Kinase InhibitorsProtein StabilityProto-Oncogene Proteins c-aktSubstrate SpecificityUbiquitin-Specific ProteasesUbiquitination