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

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

    Research output: Contribution to journalArticle

    30 Citations (Scopus)

    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 100M 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.

    Original languageEnglish
    Article number290516
    JournalJournal of Biomedicine and Biotechnology
    Volume2010
    DOIs
    Publication statusPublished - 2010

    Fingerprint

    Focal Adhesion Protein-Tyrosine Kinases
    IGF Type 1 Receptor
    Tea
    Cells
    Somatomedin Receptors
    Somatomedins
    Pancreatic Neoplasms
    Cell proliferation
    Chemical activation
    Cell Proliferation
    Cell adhesion
    Sirolimus
    Growth
    Mitogen-Activated Protein Kinases
    Cell Adhesion
    Pancreatic Carcinoma
    epigallocatechin gallate
    Apoptosis
    Therapeutics

    ASJC Scopus subject areas

    • Biotechnology
    • Molecular Medicine
    • Genetics
    • Molecular Biology
    • Health, Toxicology and Mutagenesis
    • Medicine(all)

    Cite this

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

    In: Journal of Biomedicine and Biotechnology, Vol. 2010, 290516, 2010.

    Research output: Contribution to journalArticle

    Sato, Yuko ; Vu, Hoang Anh ; Beppu, Yuuichi ; Chi, Hoang Thanh ; Sasaki, Kousuke ; Yamamoto, Hideaki ; Xinh, Phan Thi ; Tanii, Takashi ; Hara, Yukihiko ; Watanabe, Toshiki ; 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. In: Journal of Biomedicine and Biotechnology. 2010 ; Vol. 2010.
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    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 100M 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.",
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