A UBE2O-AMPKα2 Axis That Promotes Tumor Initiation and Progression Offers Opportunities for Therapy

摘要

Vila et al. show that UBE2O, which is overexpressed in many human cancers, targets AMPKα2 for ubiquitination and degradation thereby promotes activation of the mTOR-HIF1α pathway. Genetic deletion or pharmacological blockade of UBE2O inhibits tumorigenesis through the restoration of AMPKα2.