Uncoordinated 51-like kinase 2 signaling pathway regulates epithelial-mesenchymal transition in A549 lung cancer cells

Young Hwan Kim, Seung Hoon Baek, Eun Kyoung Kim, Jung Min Ha, Seo Yeon Jin, Hye Sun Lee, Hong Koo Ha, Sang Heon Song, Sun Ja Kim, Hwa Kyoung Shin, Jeongsik Yong, Do Hyung Kim, Chi Dae Kim, Sun Sik Bae

Research output: Contribution to journalArticlepeer-review

13 Scopus citations

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 languageEnglish (US)
Pages (from-to)1365-1374
Number of pages10
JournalFEBS Letters
Volume590
Issue number9
DOIs
StatePublished - May 1 2016

Bibliographical note

Funding 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).

Keywords

  • EMT
  • autophagy
  • mTORC1

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