Bcl-xL promotes metastasis independent of its anti-apoptotic activity

Bcl-xL is an anti-apoptotic protein that has also been implicated in metastasis. In this study, the authors show that nuclear Bcl-xL promotes metastasis by regulating TGFβ signaling, which is independent of the anti-apoptotic activity of Bcl-xL.

Bibliographic Details
Main Authors:	Soyoung Choi, Zhengming Chen, Laura H. Tang, Yuanzhang Fang, Sandra J. Shin, Nicole C. Panarelli, Yao-Tseng Chen, Yi Li, Xuejun Jiang, Yi-Chieh Nancy Du
Format:	Article
Language:	English
Published:	Nature Publishing Group 2016-01-01
Series:	Nature Communications
Online Access:	https://doi.org/10.1038/ncomms10384

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spelling	doaj-fff5c35ced354d01a213c99392b2ad362021-05-11T10:49:23ZengNature Publishing GroupNature Communications2041-17232016-01-017111310.1038/ncomms10384Bcl-xL promotes metastasis independent of its anti-apoptotic activitySoyoung Choi0Zhengming Chen1Laura H. Tang2Yuanzhang Fang3Sandra J. Shin4Nicole C. Panarelli5Yao-Tseng Chen6Yi Li7Xuejun Jiang8Yi-Chieh Nancy Du9Department of Pathology and Laboratory Medicine, Weill Cornell MedicineDivision of Biostatistics and Epidemiology, Department of Healthcare Policy and Research, Weill Cornell MedicineDepartment of Pathology, Memorial Sloan Kettering Cancer CenterLester and Sue Smith Breast Center, Baylor College of MedicineDepartment of Pathology and Laboratory Medicine, Weill Cornell MedicineDepartment of Pathology and Laboratory Medicine, Weill Cornell MedicineDepartment of Pathology and Laboratory Medicine, Weill Cornell MedicineLester and Sue Smith Breast Center, Baylor College of MedicineCell Biology Program, Memorial Sloan Kettering Cancer CenterDepartment of Pathology and Laboratory Medicine, Weill Cornell MedicineBcl-xL is an anti-apoptotic protein that has also been implicated in metastasis. In this study, the authors show that nuclear Bcl-xL promotes metastasis by regulating TGFβ signaling, which is independent of the anti-apoptotic activity of Bcl-xL.https://doi.org/10.1038/ncomms10384
collection	DOAJ
language	English
format	Article
sources	DOAJ
author	Soyoung Choi Zhengming Chen Laura H. Tang Yuanzhang Fang Sandra J. Shin Nicole C. Panarelli Yao-Tseng Chen Yi Li Xuejun Jiang Yi-Chieh Nancy Du
spellingShingle	Soyoung Choi Zhengming Chen Laura H. Tang Yuanzhang Fang Sandra J. Shin Nicole C. Panarelli Yao-Tseng Chen Yi Li Xuejun Jiang Yi-Chieh Nancy Du Bcl-xL promotes metastasis independent of its anti-apoptotic activity Nature Communications
author_facet	Soyoung Choi Zhengming Chen Laura H. Tang Yuanzhang Fang Sandra J. Shin Nicole C. Panarelli Yao-Tseng Chen Yi Li Xuejun Jiang Yi-Chieh Nancy Du
author_sort	Soyoung Choi
title	Bcl-xL promotes metastasis independent of its anti-apoptotic activity
title_short	Bcl-xL promotes metastasis independent of its anti-apoptotic activity
title_full	Bcl-xL promotes metastasis independent of its anti-apoptotic activity
title_fullStr	Bcl-xL promotes metastasis independent of its anti-apoptotic activity
title_full_unstemmed	Bcl-xL promotes metastasis independent of its anti-apoptotic activity
title_sort	bcl-xl promotes metastasis independent of its anti-apoptotic activity
publisher	Nature Publishing Group
series	Nature Communications
issn	2041-1723
publishDate	2016-01-01
description	Bcl-xL is an anti-apoptotic protein that has also been implicated in metastasis. In this study, the authors show that nuclear Bcl-xL promotes metastasis by regulating TGFβ signaling, which is independent of the anti-apoptotic activity of Bcl-xL.
url	https://doi.org/10.1038/ncomms10384
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Bcl-xL promotes metastasis independent of its anti-apoptotic activity

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