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.
Bibliographical noteFunding Information:
This study was supported by the Medical Research Center (MRC) Program through the National Research Foundation of Korea (NRF) grant funded by the Korea Government (MSIP) (NRF 2015R1A5A2009656), and by the National Research Foundation of Korea (NRF) grant funded by the Korea Government (MSIP) (2014R1A2A2A01004433).