| Project/Area Number |
25870554
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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 |
Dermatology
Pathological medical chemistry
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| Research Institution | Kumamoto University |
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Principal Investigator |
AOI Jun 熊本大学, 医学部附属病院, 助教 (60467991)
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2014: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2013: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 発癌 / 酸化ストレス / アンジポエチン様因子2 / 遺伝子修復機構 / 発がん / 炎症 / 加齢 / アンジオポエチン様因子２ / ミスマッチ遺伝子修復 |
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| Outline of Final Research Achievements |
Using mouse skin chemical carcinogenesis model, we reported that K14-Angptl2 Tg mice, overexpressing Angptl2 in skin epithelial cells, show enhanced susceptibility of inflammatory carcinogenesis and oxidative stress in the skin. Conversely, Angptl2 KO mice show decreased oxidative stress in skin tissue as well as a lower incidence of SCC compared with wild-type mice. In this model, treatment of K14-Angptl2 Tg mice with the antioxidant reduced oxidative stress in skin tissue and the frequency of SCC development. Interestingly, K14-Angptl2 Tg mice in the model showed significantly increased methylation of the Msh2 promoter in skin tissues. Msh2 expression in skin tissues of Tg mice was increased by antioxidant treatment, as was Msh2 promoter demethylation. Overall, this study suggests that Angptl2 accelerates carcinogenesis through increased oxidative stress and decreased Msh2 expression in skin tissue.
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