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Caffeine Inhibits the Proliferation of Liver Cancer Cells and Activates the MEK/ERK/EGFR Signalling Pathway
Author(s) -
Okano Junichi,
Nagahara Takakazu,
Matsumoto Kazuya,
Murawaki Yoshikazu
Publication year - 2008
Publication title -
basic and clinical pharmacology and toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.805
H-Index - 90
eISSN - 1742-7843
pISSN - 1742-7835
DOI - 10.1111/j.1742-7843.2008.00231.x
Subject(s) - caffeine , mapk/erk pathway , kinase , cancer research , cell growth , signal transduction , microbiology and biotechnology , chemistry , mek inhibitor , epidermal growth factor receptor , apoptosis , pharmacology , biology , receptor , endocrinology , biochemistry
Caffeine has been reported to prevent hepatocarcinogenesis. We investigated the molecular mechanisms by which caffeine inhibits the growth of hepatocellular carcinoma (HCC) cells. We found that caffeine inhibited the proliferation of HCC cells via cell cycle arrest independent of apoptosis. We revealed a novel signalling axis for caffeine involving activation of the mitogen‐activated ERK‐regulating kinase (MEK)/extracellular signal‐regulated kinase (ERK) pathway that resulted in the downstream up‐regulation of epidermal growth factor receptor (EGFR), although the MEK/ERK/EGFR signalling pathway was not involved in the growth inhibitory effect of caffeine. Our data reveal that caffeine could be a promising candidate for the treatment of patients with HCC.