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绿茶表没食子儿茶素没食子酸酯通过抑制粘着斑激酶和胰岛素样生长因子-I受体，对人胰腺癌细胞发挥抗癌作用。

Green tea epigallocatechin gallate exhibits anticancer effect in human pancreatic carcinoma cells via the inhibition of both focal adhesion kinase and insulin-like growth factor-I receptor.

作者信息

Vu Hoang Anh, Beppu Yuuichi, Chi Hoang Thanh, Sasaki Kousuke, Yamamoto Hideaki, Xinh Phan Thi, Tanii Takashi, Hara Yukihiko, Watanabe Toshiki, Sato Yuko, Ohdomari Iwao

机构信息

Consolidated Research Institute for Advanced Science and Medical Care, Waseda University, Tokyo, Japan.

出版信息

J Biomed Biotechnol. 2010;2010:290516. doi: 10.1155/2010/290516. Epub 2011 Jan 26.

DOI:10.1155/2010/290516
PMID:21318151
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3034970/
Abstract

The exact molecular mechanism by which epigallocatechin gallate (EGCG) suppresses human pancreatic cancer cell proliferation is unclear. We show here that EGCG-treated pancreatic cancer cells AsPC-1 and BxPC-3 decrease cell adhesion ability on micro-pattern dots, accompanied by dephosphorylations of both focal adhesion kinase (FAK) and insulin-like growth factor-1 receptor (IGF-1R) whereas retained the activations of mitogen-activated protein kinase and mammalian target of rapamycin. The growth of AsPC-1 and BxPC-3 cells can be significantly suppressed by EGCG treatment alone in a dose-dependent manner. At a dose of 100 μM which completely abolishes activations of FAK and IGF-1R, EGCG suppresses more than 50% of cell proliferation without evidence of apoptosis analyzed by PARP cleavage. Finally, the MEK1/2 inhibitor U0126 enhances growth-suppressive effect of EGCG. Our data suggests that blocking FAK and IGF-1R by EGCG could prove valuable for targeted therapy, which can be used in combination with other therapies, for pancreatic cancer.

摘要

表没食子儿茶素没食子酸酯（EGCG）抑制人胰腺癌细胞增殖的确切分子机制尚不清楚。我们在此表明，经EGCG处理的胰腺癌细胞AsPC-1和BxPC-3在微图案点上的细胞黏附能力降低，同时粘着斑激酶（FAK）和胰岛素样生长因子-1受体（IGF-1R）均发生去磷酸化，而丝裂原活化蛋白激酶和雷帕霉素靶蛋白的激活则得以保留。单独用EGCG处理可显著抑制AsPC-1和BxPC-3细胞的生长，且呈剂量依赖性。在100μM的剂量下，FAK和IGF-1R的激活被完全消除，EGCG抑制了超过50%的细胞增殖，通过PARP裂解分析未发现凋亡迹象。最后，MEK1/2抑制剂U0126增强了EGCG的生长抑制作用。我们的数据表明，EGCG阻断FAK和IGF-1R可能对胰腺癌的靶向治疗具有重要价值，可与其他疗法联合使用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b651/3034970/23d7c3b4ce5f/JBB2010-290516.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b651/3034970/faf3abc5750c/JBB2010-290516.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b651/3034970/b9fe9cd35ec1/JBB2010-290516.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b651/3034970/82bcb0f3ab1b/JBB2010-290516.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b651/3034970/23d7c3b4ce5f/JBB2010-290516.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b651/3034970/faf3abc5750c/JBB2010-290516.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b651/3034970/b9fe9cd35ec1/JBB2010-290516.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b651/3034970/82bcb0f3ab1b/JBB2010-290516.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b651/3034970/23d7c3b4ce5f/JBB2010-290516.004.jpg

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