Premium
Uncoordinated 51‐like kinase 2 signaling pathway regulates epithelial‐mesenchymal transition in A549 lung cancer cells
Author(s) -
Kim Young Hwan,
Baek Seung Hoon,
Kim Eun Kyoung,
Ha Jung Min,
Jin Seo Yeon,
Lee Hye Sun,
Ha Hong Koo,
Song Sang Heon,
Kim Sun Ja,
Shin Hwa Kyoung,
Yong Jeongsik,
Kim DoHyung,
Kim Chi Dae,
Bae Sun Sik
Publication year - 2016
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1002/1873-3468.12172
Subject(s) - epithelial–mesenchymal transition , gene silencing , autophagy , cancer research , microbiology and biotechnology , a549 cell , chemistry , gene knockdown , kinase , cell , biology , metastasis , cancer , biochemistry , apoptosis , genetics , gene
Epithelial‐mesenchymal transition ( EMT ) is a critical response during cancer cell metastasis. In this study, we provide evidence that uncoordinated 51‐like kinase 2 ( ULK 2) regulates EMT . Induction of autophagy by inhibition of mammalian target of rapamycin complex 1 ( mTORC 1) or by disruption of mTORC 1 by silencing raptor significantly enhanced EMT , however, disruption of mTORC 2 by silencing rictor had no effect. Knockdown of ULK 2 expression significantly induced autophagy, EMT , and migration but suppressed proliferation as well as tumor growth in a xenotransplantation model, whereas silencing of ULK 1 had no effect. Therefore, we suggest that ULK 2 regulates EMT through modulation of autophagy.