Elucidation of the mechanism of Epithelial-Mesenchymal Transition in peritoneal environment of gastric cancer
| Project/Area Number |
24791402
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Digestive surgery
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| Research Institution | Kanazawa University |
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Principal Investigator |
KINOSHITA Jun 金沢大学, 医学系, 協力研究員 (90584855)
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2012: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | 胃癌 / 腹膜播種 / 上皮間葉転換 / 腹膜中皮細胞 / PSK / EMT / 線維化 / HPMC |
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| Research Abstract |
In this study, we evaluated the mechanism of EMT of Human PeritonealMesothelial Cell(HPMC) in in peritoneal environment of gastric cancer. We also investigated the inhibitory effect of PSK on the TGF/Smad signalling pathway and TGFb induced EMT in human HPMCs and gastric cancer cells. In vitro, TGFb increased the expression of E cadherin and decreased the expression of mesenchymal markers in HPMCs and which was suppressed by PSK. PSK suppressed TGFb induced phosphorylation of Smad2 in HPMCs in western blot analysis.In mouse subctaneous xenograft models, PSK inhibited the tumor fibrosis induced by co-inoculation of gastric cancer cells and HPMCs. PSK might have the potential to reduce TGFb induced activation of HPMCs in the peritoneal microenvironment of gastric cancer.
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Report
(3 results)
Research Products
(2 results)
