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Title
  • en Involvement of STAP-2 in Brk-mediated phosphorylation and activation of STAT5 in breast cancer cells.
Creator
Accessrights open access
Rights
  • en The definitive version is available at www.blackwell-synergy.com
Subject
  • Other en Brk
  • Other en STAP-2
  • Other en STAT5
  • Other en phosphorylation
  • Other en breast cancer
  • NDC 499
Description
  • Abstract en Signal-transducing adaptor protein (STAP)-2 is a recently identified adaptor protein that contains Pleckstrin homology (PH) and Src homology 2 (SH2)-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 PH 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.
Publisher en Wiley
Date
    Issued2011-04
Language
  • eng
Resource Type journal article
Version Type AM
Identifier HDL http://hdl.handle.net/2115/48965
Relation
  • isVersionOf DOI https://doi.org/10.1111/j.1349-7006.2010.01842.x
  • PMID 21205088
Journal
    • PISSN 1347-9032
    • EISSN 1349-7006
    • NCID AA11808050
      • en Cancer Science
      • Volume Number102 Issue Number4 Page Start756 Page End761
File
Oaidate 2023-10-07