Yu Chen1, Kenan Huang1, Xinyu Ding1, Hua Tang1, Zhifei Xu1. 1. Department of Thoracic Surgery, Shanghai Changzheng Hospital, Second Military Medical University, Shanghai 200003, China.
Abstract
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.
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.
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