The Antitumor Activity Of Five Novel Lignan Compounds In SGC-7901, HepG2 And Hela Cells In Vitro

Objective: To evaluate the antitumor activity of five novel lignan compounds, and filter the compounds witch having well antitumor activity, to explore their antitumor mechanism.Methods: Using the methylthiazoly tetrazolium(MTT) assay to evaluated the cytotoxicity of Lignan1~5 against human gastric cancer cells SGC-7901, human liver cancer cells HepG2 and human cervical cancer cells Hela in intro, and half maximal(50%) inhibitory concentration(IC50) values were calculated. The morphological changes of the SGC-7901 and HepG2 cells were observed by the inverted phase contrast microscope. The cell cycle phase distribution and apoptosis were measured by flow cytometry. The expression of apoptosis associated proteins of Caspase3, Bcl-2 and Bax were determined by Western blot.Results: Lignan-1 and lignin-2 exhibited inhibitory effect on three cancer cells at the different concentration, with time- and dose-dependent manner, and the antitumor activity of lignan1 was more obvious. The IC50 of lignan-1 on SGC-7901, HepG2 and Hela cells were respectively 4.19μg/ml, 12.28μg/ml and 5.31μg/ml. The IC50 of lignan-1 on SGC-7901, HepG2 and Hela cells were respectively 14.07μg/ml, 16.20μg/ml and 9.45μg/ml. The antitumor activity of lignin3~5 were weak. Morphological examination showed that lignan-1 could destroy the SGC-7901 and HepG2 cells with the increasing concentration of lignan-1. The rate of the apoptosis cells and G2/M phase cells raised significantly after 48 hours treatment with lignan-1,as same as the expression of Caspase3 on both SGC-7901 and HepG2 and Bax on SGC-7901 only. G0/G1 phase cells on both SGC-7901 and HepG2 and Bcl-2 on SGC-7901 only decreased significantly with the increasing concentration of lignan-1.Conclusion: lignan1 and lignan2 show good antitumor activity on SGC-7901, HepG2 and Hela cells, and the antitumor activity has significant relationship with 4`-phenolic hydroxyl group. The lignan-1 could inhibit the proliferation of SGC-7901 and HepG2 cells and induce apoptosis by arresting cells at G2/M phase in vitro. The mechanisms were associated with activation of Caspase3 and Bax and inhibition of Bcl-2.