| Project/Area Number |
26461391
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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 |
Endocrinology
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| Research Institution | Prefectural University of Hiroshima (2015-2016)
Research Institute, International Medical Center of Japan (2014) |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
MINOKOSHI YASUHIKO 生理学研究所, 発達生理学研究系, 教授 (10200099)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2016: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 胃 / レプチン / 腸上皮化生 / 胃がん / 肥満 |
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| Outline of Final Research Achievements |
Dysregulation of leptin receptor (ObR) signaling have been reported to link to development of gastritis and gastric tumors. In this study, we demonstrated that ObR signaling activation is essential for the induction of gastric tumor and intestinal metaplasia, the precancerous lesions of the stomach using both model of gene-targeting and diet-induced obese mice. We found that PI3K-Akt pathway activation, intracellular accumulation of β-catenin, cancer stem cell-like cells and the essential regulators of pluripotency, following phosphorylation of ObR in the stomach. These observations were abrogated in the ObR signaling deficient mice, indicating that the homeostasis of gastric mucosal cells is responsible for cellular events downstream of ObR.
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