2016 Fiscal Year Final Research Report
The biological role and signal pathway of Stat5 in pancreatic cancer
| Project/Area Number |
26462075
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Digestive surgery
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| Research Institution | Nippon Medical School |
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Principal Investigator |
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| Research Collaborator |
Korc Murray Indiana University School of Medicine IU, Department of Medicine, Professor
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Keywords | 膵癌 / STAT5 / 接着 / 浸潤 / ゲムシタビン抵抗性 |
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| Outline of Final Research Achievements |
In our study, expressions of signal transducers and activators of transcription 5a/5b (STAT5a/5b) mRNA and protein were detected in eight kinds of pancreatic cancer cells. STAT5a/5b in pancreatic cancer cells is constitutively activated. STAT5b shRNA clones in PANC-1 cells exhibited reduced chemoresistance against gemcitabine compared to sham. STAT5b shRNA clones in PANC-1 cells were more sensitive to the proapoptotic actions of gemcitabine, as evidenced by PARP and cleaved caspase 3 activation. Gemcitabine also significantly reduced Bcl-xL levels in the STAT5b shRNA-expressing cells. STAT5a/5b shRNA clones in PANC-1 exhibited reduced adhesion, and invasion These findings suggest that STAT5b confers gemcitabine chemoresistance and STAT5a/5b promotes cell adherence and invasiveness in pancreatic cancer cells. Targeting STAT5a/5b may lead to novel therapeutic strategies for pancreatic ductal adenocarcinoma.
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| Free Research Field |
消化器外科
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