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