Plumericin inhibits growth of liver carcinoma cells via downregulation of COX-2 and VEGF

Purpose: To investigate the antitumor effect of plumericin on hepatocellular carcinoma and the underlying molecular mechanism(s). Methods: Invasion of cancer cells was measured with matrigel Transwell assay, while COX 2 and VEGF mRNA expressions were determined using quantitative polymerase chain reaction (qPCR) Results: Plumericin caused dose-dependent reductions in proliferations of Hep 3B and Hep G2 cancer cells. The degrees of proliferation of Hep 3B cells were 91, 84, 72, 57, 42 and 29 % at plumericin concentrations of 5, 10, 15, 20, 25 and 30 mu M, respectively. In Hep G2 cells plumericin treatment at doses of 5, 10, 15, 20, 25 and 30 mu M decreased proliferation to 89, 78, 64, 53, 42 and 30 %, respectively at 72 h. Treatment of Hep 3B cells at plumericin doses of 20, 25 and 30 mu M led to induction of apoptosis in 41.23, 56.76 and 68.54 % of cells, respectively after 72 h. Plumericin suppressed the invasion potential of Hep 3B cells in a dose-dependent manner. Compared to control, the proportion of Hep 3B cells in G2/M phase of cell cycle increased significantly at doses of 20, 25 and 30 mu M. Plumericin treatment of Hep 3B cells led to significant decrease in expressions of COX 2 and VEGF. Conclusion: Plumericin suppresses liver cancer cell growth in vitro and in vivo by inhibition of COX 2 and VEGF expressions. Thus, it may be used for the treatment of liver cancer.