LAUSR

Background Magnolol has shown anti-cancer activity against a variety of cancers, such as liver, breast, lung and colon cancer. However, the role of magnolol in esophagus cancer cells is unknown. Methods In this study, esophagus cancer cell lines including TE-1, Eca-109 and KYSE-150 were used to evaluate the cytotoxic effect of magnolol on cell proliferation, apoptosis and migration. Results We found that magnolol inhibits cellular proliferation of all three cell lines in a time- and dose-dependent manner; 20 µM magnolol markedly inhibited the migration ability of KYSE-150 cell which was accompanied with a decreased expression of MMP-2. Treatment with 100 µM magnolol significantly increased KYSE-150 cell apoptosis. We found that cleaved caspase-3, cleaved capsese-9 and Bax protein expression was increased and Bcl-2 protein expression was decreased after magnolol treatment. In addition, Magnolol had no effect on JNK but induced the phosphorylation of p38 and ERK1/2 in a concentration-dependent manner, suggesting the involvement of these kinases in the initiation of the apoptosis process. Finally, magnolol treatment significantly suppressed KYSE-150 tumor cell growth in nude mouse xenograft models. Conclusions The results of this study provide a basis for the understanding and development of magnolol as a potential novel drug for esophagus cancer.