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
|
Project Status |
Completed (Fiscal Year 2009)
|
Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2009: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2008: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
|
Keywords | 口腔癌 / カテキン / アポトーシス / p38 / c-Abl / MAPK |
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.
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