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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 μM, respectively. In Hep G2 cells plumericin treatment at doses of 5, 10, 15, 20, 25 and 30 μM 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 μM 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 μM. 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. Keywords: Metastasis, Aflatoxins, Plumericin, Matrigel, Cyclooxygenase

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