| Project/Area Number |
26670855
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Surgical dentistry
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| Research Institution | Hokkaido University |
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Principal Investigator |
satoh chiharu 北海道大学, 大学病院, 講師 (50222013)
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| Co-Investigator(Kenkyū-buntansha) |
HIGASHINO FUMIHIRO 北海道大学, 大学院歯学研究科, 准教授 (50301891)
KITAMURA TETSUYA 北海道大学, 大学院歯学研究科, 助教 (00451451)
MAISHI NAKO 北海道大学, 遺伝子病制御研究所, 助教 (00632423)
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| Project Period (FY) |
2014-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | PTHrP / 腫瘍微小環境 / CAF / PTHｒP |
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| Outline of Final Research Achievements |
Oral squamous cell carcinoma produce PTHrP, and PTHrP-positive cases showed a statistically significant presence of αSMA positive cancer-associated fibroblasts in the stroma. PTHrP processing was found to exacerbate proliferative activity of fibroblasts, and CAF was obtained, as seen in the expression of αSMA. The fibroblasts expressed PTH1R, a receptor of PTHrP, and PTHrP processing was found to stimulate ERK phosphorylation.
These results suggest that PTHrP produced by oral cancer tumors utilizes ERK activation with PTH/PTHrP as a receptor to induce the fibroblasts in the surrounding microenvironment to develop into CAF.
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