Cargando…

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

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...

Descripción completa

Detalles Bibliográficos
Autores principales: 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
Formato: Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2010
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3034970/
https://www.ncbi.nlm.nih.gov/pubmed/21318151
http://dx.doi.org/10.1155/2010/290516
_version_ 1782197717664006144
author 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
author_facet 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
author_sort Vu, Hoang Anh
collection PubMed
description 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.
format Text
id pubmed-3034970
institution National Center for Biotechnology Information
language English
publishDate 2010
publisher Hindawi Publishing Corporation
record_format MEDLINE/PubMed
spelling pubmed-30349702011-02-11 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 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 J Biomed Biotechnol Research Article 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. Hindawi Publishing Corporation 2010 2011-01-26 /pmc/articles/PMC3034970/ /pubmed/21318151 http://dx.doi.org/10.1155/2010/290516 Text en 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.
spellingShingle Research Article
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
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
title 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
title_full 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
title_fullStr 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
title_full_unstemmed 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
title_short 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
title_sort 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
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3034970/
https://www.ncbi.nlm.nih.gov/pubmed/21318151
http://dx.doi.org/10.1155/2010/290516
work_keys_str_mv AT vuhoanganh greenteaepigallocatechingallateexhibitsanticancereffectinhumanpancreaticcarcinomacellsviatheinhibitionofbothfocaladhesionkinaseandinsulinlikegrowthfactorireceptor
AT beppuyuuichi greenteaepigallocatechingallateexhibitsanticancereffectinhumanpancreaticcarcinomacellsviatheinhibitionofbothfocaladhesionkinaseandinsulinlikegrowthfactorireceptor
AT chihoangthanh greenteaepigallocatechingallateexhibitsanticancereffectinhumanpancreaticcarcinomacellsviatheinhibitionofbothfocaladhesionkinaseandinsulinlikegrowthfactorireceptor
AT sasakikousuke greenteaepigallocatechingallateexhibitsanticancereffectinhumanpancreaticcarcinomacellsviatheinhibitionofbothfocaladhesionkinaseandinsulinlikegrowthfactorireceptor
AT yamamotohideaki greenteaepigallocatechingallateexhibitsanticancereffectinhumanpancreaticcarcinomacellsviatheinhibitionofbothfocaladhesionkinaseandinsulinlikegrowthfactorireceptor
AT xinhphanthi greenteaepigallocatechingallateexhibitsanticancereffectinhumanpancreaticcarcinomacellsviatheinhibitionofbothfocaladhesionkinaseandinsulinlikegrowthfactorireceptor
AT taniitakashi greenteaepigallocatechingallateexhibitsanticancereffectinhumanpancreaticcarcinomacellsviatheinhibitionofbothfocaladhesionkinaseandinsulinlikegrowthfactorireceptor
AT harayukihiko greenteaepigallocatechingallateexhibitsanticancereffectinhumanpancreaticcarcinomacellsviatheinhibitionofbothfocaladhesionkinaseandinsulinlikegrowthfactorireceptor
AT watanabetoshiki greenteaepigallocatechingallateexhibitsanticancereffectinhumanpancreaticcarcinomacellsviatheinhibitionofbothfocaladhesionkinaseandinsulinlikegrowthfactorireceptor
AT satoyuko greenteaepigallocatechingallateexhibitsanticancereffectinhumanpancreaticcarcinomacellsviatheinhibitionofbothfocaladhesionkinaseandinsulinlikegrowthfactorireceptor
AT ohdomariiwao greenteaepigallocatechingallateexhibitsanticancereffectinhumanpancreaticcarcinomacellsviatheinhibitionofbothfocaladhesionkinaseandinsulinlikegrowthfactorireceptor