| Project/Area Number |
15K08118
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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 |
Medical pharmacy
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| Research Institution | Mukogawa Women's University |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
YAMAMORI Motohiro 武庫川女子大学, 薬学部, 講師 (10444613)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2017: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | 膵臓がん / PPARγ / アポトーシス / 創薬ターゲット / troglitazone / ERCC1 |
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| Outline of Final Research Achievements |
When mechanisms of effects of troglitazone on human pancreatic cancer cell lines were investigated, troglitazone exhibited increases of chromatin condensation, caspase 3 activities and Bax/Bcl expression ratio, suggesting caspase-dependent apoptosis. Also, it was suggested that JNK pathway was involved in the apoptosis. In addition, ERCC1, a key protein in the pathway of DNA repair, were decreased by troglitazone treatment. Synergistic effects of troglitazone and a platinum drug were observed but no change of ERCC1 expression was observed. It was suggested that another mechanism could be involved in the synergistic effects.
In addition, tumor growth in the xenograft model was inhibited by oral administration of troglitazone.
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