| Project/Area Number |
23590404
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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 |
Human pathology
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| Research Institution | Sapporo Medical University |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
MURATA Masaki 札幌医科大学, 医学部, 講師 (10404592)
TAKASAWA Akira 札幌医科大学, 医学部, 助教 (00593021)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2013: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2012: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2011: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | ヒト正常膵管上皮細胞 / 膵癌 / 分子標的治療 / PKC / claudin / 抗癌剤 / タイト結合 |
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| Research Abstract |
In the present study, using normal human pancreatic duct epithelial cells and cancer cell lines. we investigated the basic study targeting tight junction molecules claudin-4, -18 and a signal molecule PKC that highly expressed in pancreatic cancer. Claudin-4 and -18 were regulated via a PKCalpha signal transduction pathway in both human pancreatic duct epithelial cells and cancer cells. The cytotoxic effects of CPE via claudin-4 are thought to be useful as a novel therapeutic tool for pancreatic cancer. The cytotoxicity was not observed at any concentration of CPE, whereas in pancreatic cancer cells, CPE had a dose-dependent cytotoxic effect. PKCalpha inhibitors represent potential therapeutic agents against human pancreatic cancer cells by the use of CPE cytotoxicity via claudin-4.
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