2005 Fiscal Year Final Research Report Summary
Analysis of the mechanisms of cell proliferation by T-caclherin in skin prolit~rative diseases
Project/Area Number |
16591097
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Dermatology
|
Research Institution | Kyoto University |
Principal Investigator |
MATSUYISHI Norihisa Kyoto University, Graduate School of Medicine, Lecturer, 医学研究科, 講師 (10263071)
|
Co-Investigator(Kenkyū-buntansha) |
TODA Ken-ichi Kitano Hospital, Department of Dermatology, Director, 北野病院・皮膚科, 部長 (80159045)
|
Project Period (FY) |
2004 – 2005
|
Keywords | T-cadherin / inhibition of cell proliferation / suqamous cell carcinoma / transfection / RNA interference / cell cycle |
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.
|
Research Products
(2 results)