2017 Fiscal Year Final Research Report
PP6 as a tumor suppressor in mouse two-stage chemical carcinogenesis
Project/Area Number |
15K10081
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
General surgery
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Research Institution | Miyagi Prefectural Hospital Organization Miyagi Cancer Center |
Principal Investigator |
KAKUGAWA Yoichiro 地方独立行政法人宮城県立病院機構宮城県立がんセンター(研究所), がん薬物療法研究部, 特任研究員 (60221173)
|
Co-Investigator(Kenkyū-buntansha) |
島 礼 地方独立行政法人宮城県立病院機構宮城県立がんセンター(研究所), がん薬物療法研究部, 部長 (10196462)
佐藤 郁郎 地方独立行政法人宮城県立病院機構宮城県立がんセンター(研究所), ティッシュバンクセンター, 部長 (50225918)
|
Project Period (FY) |
2015-04-01 – 2018-03-31
|
Keywords | 紫外線発がん / プロテインホスファターゼ |
Outline of Final Research Achievements |
Recently, to determine whether PP6 deficiency functions in carcinogenesis in vivo, we employed a mouse skin 2-stage carcinogenesis model. We found that a single DMBA application was sufficient to produce papillomas in Ppp6c-deficient skin. As such, ours was the first report that Ppp6c loss-of-function acts as a tumor promoter in mice. Here, we investigated effect of UVB radiation on mouse keratinocytes in which Ppp6c had been deleted. Following UVB irradiation, mice with Ppp6c-deficient keratinocytes showed a higher incidence of skin squamous cell carcinoma than did control mice. We concluded that Ppp6c loss-of-function in mouse skin showed hypersensitivity to UVB-induced squamous cell carcinoma. Our histochemical analyses suggest that Ppp6c deficiency underlies molecular events that drive outgrowth of initiated keratinocytes harboring UVB-induced mutated p53.
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Free Research Field |
医歯薬学
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