Analysis of the mechanisms of cell proliferation by T-caclherin in skin prolit~rative diseases
| Project/Area Number |
16591097
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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 | Kyoto University |
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Principal Investigator |
MATSUYISHI Norihisa Kyoto University, Graduate School of Medicine, Lecturer, 医学研究科, 講師 (10263071)
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| Co-Investigator(Kenkyū-buntansha) |
TODA Ken-ichi Kitano Hospital, Department of Dermatology, Director, 北野病院・皮膚科, 部長 (80159045)
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| Project Period (FY) |
2004 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2005: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 2004: ¥2,600,000 (Direct Cost: ¥2,600,000)
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| Keywords | T-cadherin / inhibition of cell proliferation / suqamous cell carcinoma / transfection / RNA interference / cell cycle / 増殖抑制 / 扁平上皮癌細胞株 |
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| Research Abstract |
T-cadherin is a unique member of cadherin superfamily that lacks transmembrane daomain and cytoplasmic domain. And instead of those domains, it linked to the plasma membrane via a glycosyl-phoshatidylinositol anchor. Cytoplasmic domain of classical cadherin is crucial for its cell-cell adhesion, and the lack in T-cadherin means the existence of another function except for adhesion. The fact that T-cadherin expression is downregulated in cell proliferative disorders including squamous carcinoma or psoriasis vulgaris suggests that T-cadherin is associated with cell proliferation. In this study, we established two kinds of cell lines. One is T-cadherin overexpressed human squamous carcinoma cell line (HSC-1) by transfection method and another is T-cadherin knock down HSC-1 by RNAi method. We anlysed the effect of T-cadherin on proliferation using previous cell lines and intact HSC-1 cells, and found that T-cadherin was negative regulator of cell proliferation. We also confirmed the result using tetracycline inducible trasfectant. This function was cased by the dely of cell proliferation cycle at G2/M phase. These results suggets that T-cadherin is a key molecule of cell proliferation mechanisms in human squamous carcinoma cells.
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Report
(3 results)
Research Products
(4 results)
