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

绿茶儿茶素通过MAPK信号通路诱导人口腔癌细胞凋亡的机制

• 批准号: 20791330
• 负责人: KAGAYA Noritaka
• 金额: $ 2.41万
• 依托单位: Tokyo Medical and Dental University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Young Scientists (B)
• 财政年份: 2008
• 资助国家: 日本
• 起止时间: 2008 至 2009
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-20791330/
• 关键词: 口腔癌; カテキン; アポトーシス; p38; c-Abl; MAPK

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.

在本研究中，我研究了EGCG（一种绿色茶儿茶素）诱导人口腔癌细胞株凋亡的机制。经EGCG处理后，ZA细胞中PARP和caspase被激活，同时MAPK p38被激活。已知非受体酪氨酸激酶c-Abl特异性激活MAPK p38。因此，使用c-Abl抑制剂伊马替尼或c-Abl shRNA检查c-Abl在EGCG诱导的细胞凋亡中的作用。抑制c-Abl信号传导可有效抑制EGCG诱导的ZA细胞凋亡。此外，c-Abl的核定位观察后，EGCG处理。在未被EGCG诱导凋亡的HSC 4细胞中，转染c-Abl基因后，被EGCG诱导凋亡。提示c-Abl在EGCG诱导的细胞凋亡中起重要作用。

项目成果

ヒト口腔癌細胞に対する緑茶カテキンの細胞死誘導機構

绿茶儿茶素诱导人口腔癌细胞死亡的机制

• 发表时间: 2008
• 作者: 加賀谷紀貴;原征彦
• 通讯作者: 原征彦

口腔癌細胞において緑茶カテキンが誘導するc-Ablを介するアポトーシスシグナル

绿茶儿茶素诱导的c-Abl介导的口腔癌细胞凋亡信号

• 发表时间: 2009
• 作者: 蔭山晶子、河合建一郎;他;二木元典;二木元典;二木元典;二木元典;二木元典;加賀谷紀貴
• 通讯作者: 加賀谷紀貴