| Project/Area Number |
15K19903
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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 | Kyoto Prefectural University of Medicine |
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Principal Investigator |
Kosuga Toshiyuki 京都府立医科大学, 医学(系)研究科(研究院), 助教 (00457946)
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| Project Period (FY) |
2015-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2016: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | アクアポリン5 / 胃癌 / 肝癌 / 温熱刺激 / 低浸透圧刺激 / 細胞周期 |
|---|
| Outline of Final Research Achievements |
Recent studies have shown that aquaporin5 (AQP5) is expressed in various cancers, and plays a role in tumor progression. We herein examined whether heat shock exerts anticancer effects via the changes in AQP5 expression. The expression of AQP5 protein was high in Alexander cells, a human liver cancer cell line. Heat shock decreased AQP5 on cellular membranes and in the cytoplasm of Alexander cells, and suppressed cell migration/invasion and proliferation, and induced early apoptosis and G0/G1 arrest. Meanwhile, the knockdown of AQP5 using AQP5-siRNA similarly suppressed cell migration/invasion and proliferation, and induced early apoptosis and G0/G1 arrest. Cycloheximide (CHX) chase experiments revealed that heat shock accelerated the degradation of AQP5, which was rescued under CHX and the autophagy inhibitor, bafilomycin A1. In conclusion, heat shock induces anticancer effects on liver cancer via the autophagic degradation of AQP5 on the cellular membrane and in the cytoplasm.
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