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

doi:10.1002/1873-3468.12172

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

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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	https://doi.org/10.1002/1873-3468.12172
State	Published - May 1 2016

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Publisher Copyright:
© 2016 Federation of European Biochemical Societies.

Keywords

EMT
autophagy
mTORC1

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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

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.",

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

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AU - Kim, Young Hwan

AU - Baek, Seung Hoon

AU - Kim, Eun Kyoung

AU - Ha, Jung Min

AU - Jin, Seo Yeon

AU - Lee, Hye Sun

AU - Ha, Hong Koo

AU - Song, Sang Heon

AU - Kim, Sun Ja

AU - Shin, Hwa Kyoung

AU - Yong, Jeongsik

AU - Kim, Do Hyung

AU - Kim, Chi Dae

AU - Bae, Sun Sik

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AB - 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.

KW - EMT

KW - autophagy

KW - mTORC1

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

Abstract

Bibliographical note

Keywords

UN SDGs

Access

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