FEBS Letters · 2016 · 38 citations · 30 references
Life SciencesCell BiologyOncologyAutophagyMetastasisSignal TransductionAutophagy RegulationCancer Cell SignalingCancer ProgressionEpithelial-mesenchymal TransitionEpithelial-to-mesenchymal TransitionSignal Transduction In CancerAutophagy Regulation By Mtor Complex 1Cancer Metastasis MechanismsCancer-associated AutophagyCell XenotransplantationEpithelial TransitionEpithelial-mesenchymal Transition In CancerMtorc1 SignalingTumor Growth Dynamics
Epithelial-mesenchymal transition (EMT) is a critical response during cancer cell metastasis. In this study, we provide evidence that uncoordinated 51-like kinase 2 (ULK2) regulates EMT. Induction of autophagy by inhibition of mammalian target of rapamycin complex 1 (mTORC1) or by disruption of mTORC1 by silencing raptor significantly enhanced EMT, however, disruption of mTORC2 by silencing rictor had no effect. Knockdown of ULK2 expression significantly induced autophagy, EMT, and migration but suppressed proliferation as well as tumor growth in a xenotransplantation model, whereas silencing of ULK1 had no effect. Therefore, we suggest that ULK2 regulates EMT through modulation of autophagy.
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