| Project/Area Number |
21591437
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Dermatology
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| Research Institution | Kyushu University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
TAKAHARA Masakazu 九州大学, 大学病院, 講師 (20398093)
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| Project Period (FY) |
2009 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2011: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2010: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2009: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 皮膚悪性腫瘍 / CD10 / Snail / EMT / 線維芽細胞 / SATB1 / アルギナーゼ / サイトケラチン / サイトカイン / カテプシンK |
|---|
| Research Abstract |
We demonstrated that IL-1αproduction by cutaneous squamous cell carcinoma(SCC) induced CD10 expression in the stromal fibroblast. The CD10-bearing fibroblast inhibited the invasive capacity of SCC by diminishing the microenvironmental concentration of substance P that supports tumor invasion via metalloproteinase induction.
Cathepsin K expression was detected in peritumoral fibroblasts around SCC, but not in those surrounding benign epidermal tumors. The CTSK-upregulated fibroblasts generated by SCC-derived IL-1αaugmented the matrigel invasive ability of SCC cells.
Taken together, these results highlighted the novel mechanism of stromal fibroblast playing important roles in cutaneous SCC invasion.
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