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Journal of Biomedicine and Biotechnology
Volume 2010 (2010), Article ID 290516, 8 pages
http://dx.doi.org/10.1155/2010/290516
Research Article

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

1Consolidated Research Institute for Advanced Science and Medical Care (ASMeW), Waseda University, Tokyo 169-8050, Japan
2Division of Ultrafine Structure, Department of Pathology, Research Institute of International Medical Center of Japan, Toyama 1-21-1, Shinjuku-ku, Tokyo 162-8655, Japan
3Faculty of Science and Engineering, Waseda University, Tokyo 169-8555, Japan
4Department of Medical Genome Sciences, Graduate School of Frontier Sciences, The University of Tokyo, Tokyo 108-8639, Japan
5Tea Solutions, Food Research Lab, Hara Office Inc, Miyabara, Fujieda City 130-0012, Japan

Received 10 November 2010; Accepted 29 December 2010

Academic Editor: Gary E. Gallick

Copyright © 2010 Hoang Anh Vu et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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.