Abstract
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.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 1365-1374 |
| Number of pages | 10 |
| Journal | FEBS Letters |
| Volume | 590 |
| Issue number | 9 |
| DOIs | |
| State | Published - May 1 2016 |
Bibliographical note
Publisher Copyright:© 2016 Federation of European Biochemical Societies.
UN SDGs
This output contributes to the following UN Sustainable Development Goals (SDGs)
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SDG 3 Good Health and Well-being
Keywords
- EMT
- autophagy
- mTORC1
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