Involvement of STAP-2 in Brk-mediated phosphorylation and activation of STAT5 in breast cancer cells

Osamu Ikeda, Akihiro Mizushima, Yuichi Sekine, Chikako Yamamoto, Ryuta Muromoto, Asuka Nanbo, Kenji Oritani, Akihiko Yoshimura, Tadashi Matsuda

Research output: Contribution to journalArticlepeer-review

16 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)756-761
Number of pages6
JournalCancer science
Volume102
Issue number4
DOIs
Publication statusPublished - 2011 Apr

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

Fingerprint Dive into the research topics of 'Involvement of STAP-2 in Brk-mediated phosphorylation and activation of STAT5 in breast cancer cells'. Together they form a unique fingerprint.

Cite this