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J Biomed Biotechnol ; 2010: 290516, 2010.
Artigo em Inglês | MEDLINE | ID: mdl-21318151

RESUMO

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.


Assuntos
Antineoplásicos/farmacologia , Catequina/análogos & derivados , Quinase 1 de Adesão Focal/antagonistas & inibidores , Neoplasias Pancreáticas/metabolismo , Receptor IGF Tipo 1/antagonistas & inibidores , Chá , Antineoplásicos/uso terapêutico , Antioxidantes/metabolismo , Antioxidantes/farmacologia , Apoptose/fisiologia , Catequina/metabolismo , Catequina/farmacologia , Catequina/uso terapêutico , Linhagem Celular Tumoral , Proliferação de Células/efeitos dos fármacos , Relação Dose-Resposta a Droga , Ativação Enzimática/efeitos dos fármacos , Humanos , Proteínas Quinases Ativadas por Mitógeno/metabolismo , Neoplasias Pancreáticas/tratamento farmacológico
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