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

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

doi:10.1038/ncomms10384

Nature Communications (Jan 2016)

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

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

Affiliations

Soyoung Choi: Department of Pathology and Laboratory Medicine, Weill Cornell Medicine
Zhengming Chen: Division of Biostatistics and Epidemiology, Department of Healthcare Policy and Research, Weill Cornell Medicine
Laura H. Tang: Department of Pathology, Memorial Sloan Kettering Cancer Center
Yuanzhang Fang: Lester and Sue Smith Breast Center, Baylor College of Medicine
Sandra J. Shin: Department of Pathology and Laboratory Medicine, Weill Cornell Medicine
Nicole C. Panarelli: Department of Pathology and Laboratory Medicine, Weill Cornell Medicine
Yao-Tseng Chen: Department of Pathology and Laboratory Medicine, Weill Cornell Medicine
Yi Li: Lester and Sue Smith Breast Center, Baylor College of Medicine
Xuejun Jiang: Cell Biology Program, Memorial Sloan Kettering Cancer Center
Yi-Chieh Nancy Du: Department of Pathology and Laboratory Medicine, Weill Cornell Medicine

DOI: https://doi.org/10.1038/ncomms10384
Journal volume & issue: Vol. 7, no. 1
pp. 1 – 13

Abstract

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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.

Published in Nature Communications

ISSN: 2041-1723 (Online)
Publisher: Nature Portfolio
Country of publisher: United Kingdom
LCC subjects: Science
Website: https://www.nature.com/ncomms/

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