| Project/Area Number |
15K19905
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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 |
Konishi Hirotaka 京都府立医科大学, 医学(系)研究科(研究院), 助教 (00448739)
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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 | 食道癌 / オートファジー / Nrf2 / 化学療法 / Ｎｒｆ２ / 抗がん剤感受性 / 治療抵抗性 |
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| Outline of Final Research Achievements |
The aim of this research is an establishment of a novel therapeutic strategy according to the state of autophagy in esophageal carcinoma. It was confirmed that decrease of ATG7 expression, which is the main gene of autophagy flux, associated with the suppression of autophagy or worse prognosis. Moreover, the restoration of ATG7 expression and autophagy flux lead the suppression of p62 protein expression due to the autophagy specific degradation. This suppression of p62 protein lead the degradation or destabilization of Nrf2, which is the main factor of cellular protection, and now the effects for cancer cells or prognosis due to the decrease of Nrf2 protein are being investigated.
On the other hands, the degradation of AQP5 protein is likely to be caused by autophagy specific degradation. It was reported that autophagy is associated with the specific degradation of AQP5 and anticancer effect in hepatocellular carcinoma.
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