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Epigallocatechin-3-gallate-induced growth inhibition and the underlying mechanisms in human hepatocellular carcinoma cells
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Abstract:
Objective :To investigate the effect of Epigallocatechin-3-gallate (EGCG) on hepatocellular carcinoma cell growth and the molecular mechanisms underlying the effect in vitro. Methods: Three human hepatocellular carcinoma cell lines (i.e., HepG2, Sk-hep1 and SMMC7721) were used in this study. Cells were cultured in the presence of 0, 40, 80 or 120 μg/ml EGCG. At 24, 48 and 72 h after EGCG treatment, cell viability was assessed by MTT assay, apoptosis by AO/EB staining, cell cycle progression by flow cytometer, and mRNA and protein levels of HO11, IL-10 and TNF-α by Realtime PCR and Western blotting respectively. Results: EGCG treatment significantly induced cell attachment (P<005), increased the proportion of apoptotic cells (P<0.01), and induced G2/M arrest (P<0.01) in all three cell lines tested as compared with the control. HO-1, IL-10 and TNF-α mRNA levels were 0.58±0.15, 5.91±1.11 and 529±1.14 in EGCG-treated Sk-hep1 cells, significantly different from the levels in the control cells (P＝0.008, P＝0002, P＝0.003). EGCG resulted in a significant decrease in HO-1 protein content as compared with the control (0.16±0.04 vs 0.33±0.08, P<0.05). In contrast, EGCG significantly increased levels of IL-10 protein (0.42± 006 vs 0.24±0.08, P<0.05) and TNF-α protein (0.95±0.17 vs 0.58±0.08, P<0.05). Conclusions: EGCG may inhibit proliferation and block cell cycle progression and induce apoptosis in hepatocellular carcinoma cells. The mechanism(s) underlying these effects of EGCG may involve modulation of HO-1, IL-10 and TNF-α expression.
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Project Supported:
Project supported by the Youth Science Foundation of Guangxi Medical University (No. 02602211011), the Guangxi Natural Science Foundation (No. 2013GXNSFBA019186), and the Scientific Research and Technological Development Program of Guangxi (No.1140003A-32)
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