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

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.
AuthorsOsamu Ikeda, Akihiro Mizushima, Yuichi Sekine, Chikako Yamamoto, Ryuta Muromoto, Asuka Nanbo, Kenji Oritani, Akihiko Yoshimura, Tadashi Matsuda
JournalCancer science (Cancer Sci) Vol. 102 Issue 4 Pg. 756-61 (Apr 2011) ISSN: 1349-7006 [Electronic] England
PMID21205088 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Copyright© 2011 Japanese Cancer Association.
Chemical References
  • Adaptor Proteins, Signal Transducing
  • Neoplasm Proteins
  • Phosphoproteins
  • RNA, Small Interfering
  • STAP2 protein, human
  • STAT3 Transcription Factor
  • STAT3 protein, human
  • Tyrosine
  • Protein-Tyrosine Kinases
  • PTK6 protein, human
Topics
  • Adaptor Proteins, Signal Transducing (antagonists & inhibitors, genetics, metabolism)
  • Blotting, Western
  • Breast Neoplasms
  • Cell Proliferation
  • Female
  • Humans
  • Immunoprecipitation
  • Neoplasm Proteins (antagonists & inhibitors, genetics, metabolism)
  • Phosphoproteins (antagonists & inhibitors, genetics, metabolism)
  • Phosphorylation
  • Promoter Regions, Genetic (genetics)
  • Protein-Tyrosine Kinases (antagonists & inhibitors, genetics, metabolism)
  • RNA, Small Interfering (genetics)
  • STAT3 Transcription Factor (genetics, metabolism)
  • Tumor Cells, Cultured
  • Tyrosine (metabolism)

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