Basic & Clinical Pharmacology & Toxicology · 2008 · 94 citations · 21 references
MedicineOncologyPharmacologyApoptosisCancer PharmacologyMolecular OncologyApoptosis In CancerApoptosis RegulationCancer Cell SignalingLiver CancerMalignant NeoplasmsOncogenic Signaling PathwaysCancer Signaling PathwaysCell Cycle InhibitionEgfr InhibitionEpidermal Growth Factor Receptor InhibitionEpidermal Growth Factor Receptor SignalingErk SignalingExtracellular Signal-regulated Kinase PathwayExtracellular Signal-regulated Kinase Signaling
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.
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