2009 Fiscal Year Final Research Report

Mechanism of green tea catechin-induced apoptosis through MAPK signaling pathway in human oral cancer cells

Research Project

Project/Area Number	20791330
Research Category	Grant-in-Aid for Young Scientists (B)
Allocation Type	Single-year Grants
Research Field	Morphological basic dentistry
Research Institution	Tokyo Medical and Dental University
Principal Investigator	KAGAYA Noritaka Tokyo Medical and Dental University, 大学院・医歯学総合研究科, 助教 (40372437)
Project Period (FY)	2008 – 2009
Keywords	口腔癌 / カテキン / アポトーシス / p38 / c-Abl
Research Abstract	In the present study, I examined the mechanism of EGCG (a green tea catechin)-induced apoptosis in human oral cancer cell lines. After EGCG treatment, PARP and caspases were activated accompanied with MAPK p38 activation in ZA cell. A non-receptor tyrosine kinase c-Abl is known to activate MAPK p38 specifically. Therefore, role of c-Abl in EGCG-induced cell apoptosis was examined using c-Abl inhibitor imatinib or c-Abl shRNA. Inhibition of c-Abl signaling effectively suppressed EGCG-induced apoptosis in ZA cell. In addition, nuclear localization of c-Abl was observed after EGCG treatment. In HSC4 cell in which apoptosis was not induced by EGCG, apoptosis was provoked by EGCG after the transfection of c-Abl gene. In conclusion, it was suggested that c-Abl have important roles in EGCG-induced cell apoptosis.