Aim: To investigate the effects of (-)-epigallocatechin-3-gallate (EGCG), an active compound in green tea, on prostaglandin E 2 (PGE 2 )-induced proliferation and migration, and the expression of prostanoid EP 1 receptors in hepatocellular carcinoma (HCC) cells. Methods: HCC cell line HepG2, human hepatoma cell lines MHCC-97L, MHCC-97H and human hepatocyte cell line L02 were used. Cell viability was analyzed using MTT assay. PGE 2 production was determined with immunoassay. Wound healing assay and transwell filter assay were employed to assess the extent of HCC cell migration. The expression of EP 1 receptor and Gq protein were examined using Western blot assay. Results: PGE 2 (4-40000 nmol/L) or the EP 1 receptor agonist ONO-DI-004 (400-4000 nmol/L) increased the viability and migration of HepG2 cells in concentration-dependent manners. EGCG (100 μg/mL) significantly inhibited the viability and migration of HepG2 cells induced by PGE 2 or ONO-DI-004. HepG2 cells secreted an abundant amount of PGE 2 into the medium, and EGCG (100 μg/mL) significantly inhibited the PGE 2 production and EP 1 receptor expression in HepG2 cells. EGCG (100 μg/mL) also inhibited the viability of MHCC-97L cells, but not that of MHCC-97H cells. Both EGCG (100 μg/mL) and EP 1 receptor antagonist ONO-8711 inhibited PGE 2 4 μmol/L and ONO-DI-004 400 nmol/L-induced growth and migration of HepG2 cells. Both EGCG (100 μg/mL) and ONO-8711 210 nmol/L inhibited PGE 2 -and ONO-DI-004-induced EP 1 expression. EGCG and ONO-8711 had synergistic effects in inhibiting EP 1 receptor expression. PGE 2 , ONO-DI-004, ONO-8711, and EGCG had no effects on Gq expression in HepG2 cells, respectively. Conclusion: These findings suggest that the anti-HCC effects of EGCG might be mediated, at least partially, through the suppressing EP 1 receptor expression and PGE 2 production.