Volume 102, Issue 4 pp. 756-761
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Involvement of STAP-2 in Brk-mediated phosphorylation and activation of STAT5 in breast cancer cells

Osamu Ikeda

Osamu Ikeda

Department of Immunology, Graduate School of Pharmaceutical Sciences Hokkaido University, Sapporo

These authors contributed equally to this work.

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Akihiro Mizushima

Akihiro Mizushima

Department of Immunology, Graduate School of Pharmaceutical Sciences Hokkaido University, Sapporo

These authors contributed equally to this work.

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Yuichi Sekine

Yuichi Sekine

Department of Immunology, Graduate School of Pharmaceutical Sciences Hokkaido University, Sapporo

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Chikako Yamamoto

Chikako Yamamoto

Department of Immunology, Graduate School of Pharmaceutical Sciences Hokkaido University, Sapporo

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Ryuta Muromoto

Ryuta Muromoto

Department of Immunology, Graduate School of Pharmaceutical Sciences Hokkaido University, Sapporo

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Asuka Nanbo

Asuka Nanbo

Department of Immunology, Graduate School of Pharmaceutical Sciences Hokkaido University, Sapporo

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Kenji Oritani

Kenji Oritani

Department of Hematology and Oncology, Graduate School of Medicine, Osaka University, Osaka

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Akihiko Yoshimura

Akihiko Yoshimura

Department of Microbiology and Immunology, Keio University School of Medicine, Tokyo, Japan

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Tadashi Matsuda

Corresponding Author

Tadashi Matsuda

Department of Immunology, Graduate School of Pharmaceutical Sciences Hokkaido University, Sapporo

To whom correspondence should be addressed.
E-mail: [email protected]Search for more papers by this author
First published: 23 December 2010
Citations: 27

Abstract

Signal-transducing adaptor protein (STAP)-2 is a recently identified adaptor protein that contains Pleckstrin homology and Src homology 2-like domains, and is also known to be a substrate of breast tumor kinase (Brk). In a previous study, we found that STAP-2 upregulated Brk-mediated activation of signal transducer and activator of transcription (STAT) 3 in breast cancer cells. Here, we examined the involvement of STAP-2 in Brk-mediated STAT5 activation in breast cancer cells. Ectopic expression of STAP-2 induced Brk-mediated transcriptional activity of STAT5. Furthermore, STAP-2-knockdown in T47D breast cancer cells induced a marked decrease in proliferation that was as strong as that after Brk- or STAT5b-knockdown. Regarding the mechanism, the Pleckstrin homology domain of STAP-2 is likely to participate in the process by which Brk phosphorylates and activates STAT5. Taken together, our findings provide insights toward the development of novel therapeutic strategies as well as novel prognostic values in breast carcinomas. (Cancer Sci 2011; 102: 756–761)

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