OBJECTIVE: To investigate the effects of matrine on proliferation, cell cycle, apoptosis rate and beta-catenin-dependent transcriptional activity in cultured hepatoma cell line Hep3B. METHODS: Cell viability was analyzed by cell counting kit-8 (CCK-8) assay. Cell cycle and apoptosis rate wene determined by flow cytometry analysis, beta-catenin-dependent transcriptional activity was assayed with Dual-Luciferase Reporter System. RESULTS: 72 h of matrine (50 - 800 mg/L) exposure significantly suppresses Hep3B cells growth in a concentration-dependent manner (P<0.01), the 50 percent inhibitory concentration (IC50) was 312.53 mg/L. A higher proportion of apoptotic cells in matrine-treated group than in control groups (21.73 +/- 1.66% vs. 4.39 +/- 1.93%) are shown. Cell proportions in G0/G1 phase were respectively 74.48% and 57.39% in matrine-treated group and control group. Cell proportions in S phase wene respectively 12.94% and 27.67%. Beta-catenin reporter activity was also decreased by matrine treatment in a concentration-dependent manner in Hep3B cells (P<0.05 or P<0.01). CONCLUSION: Through inhibition of beta-catenin-dependent transcription, matrine induces cell cycle arrest and apoptosis, and subsequently suppresses proliferation of hepatoma cells.
OBJECTIVE: To investigate the effects of matrine on proliferation, cell cycle, apoptosis rate and beta-catenin-dependent transcriptional activity in cultured hepatoma cell line Hep3B. METHODS: Cell viability was analyzed by cell counting kit-8 (CCK-8) assay. Cell cycle and apoptosis rate wene determined by flow cytometry analysis, beta-catenin-dependent transcriptional activity was assayed with Dual-Luciferase Reporter System. RESULTS: 72 h of matrine (50 - 800 mg/L) exposure significantly suppresses Hep3B cells growth in a concentration-dependent manner (P<0.01), the 50 percent inhibitory concentration (IC50) was 312.53 mg/L. A higher proportion of apoptotic cells in matrine-treated group than in control groups (21.73 +/- 1.66% vs. 4.39 +/- 1.93%) are shown. Cell proportions in G0/G1 phase were respectively 74.48% and 57.39% in matrine-treated group and control group. Cell proportions in S phase wene respectively 12.94% and 27.67%. Beta-catenin reporter activity was also decreased by matrine treatment in a concentration-dependent manner in Hep3B cells (P<0.05 or P<0.01). CONCLUSION: Through inhibition of beta-catenin-dependent transcription, matrine induces cell cycle arrest and apoptosis, and subsequently suppresses proliferation of hepatoma cells.