Artesunate induces apoptosis and inhibits growth of Eca109 and Ec9706 human esophageal cancer cell lines in vitro and in vivo

Author：

Publisher： Spandidos Publications

E-ISSN： 1791-3004|12|1|1465-1472

ISSN： 1791-2997

Source： Molecular Medicine Reports, Vol.12, Iss.1, 2015-01, pp. : 1465-1472

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Abstract

Esophageal cancer is a common malignant tumor worldwide with a high incidence rate in China and it is a great threat to human health. Combined modality therapy is used for chemotherapeutic treatment of esophageal cancer; however, drug resistance and side effects of the drugs is a major barrier to the success of chemotherapy. As chemotherapy with common drugs is far from providing satisfactory clinical outcomes for patients with esophageal cancer, more efficient drugs are urgently required. Artesunate (Art) is the firstline treatment option for malaria; however, it was recently revealed that Art has remarkable antitumor activity, making it a novel candidate for cancer chemotherapy. Although the anticancer effects of Art have been well documented, its potential against esophageal cancer has rarely been explored. The present study aimed to investigate the significance and mechanism of the antiproliferative activity of Art on esophageal cancer cells in vitro and in vivo. In the in vitro experiments, Art inhibited the growth as well as induced cell apoptosis and cell cycle arrest of esophageal cancer cell lines (Eca109 and Ec9706) in a concentrationdependent manner. Furthermore, downregulation of mitochondrial membrane potential, Bcell lymphoma2 (BCL2) and CDC25A, as well as upregulation of BCL2associated X protein (Bax) and caspase3 expression in Arttreated cells were identified. In addition, an in vivo study showed that Art produced a dosedependent tumor regression in nude mice, while side effects were low. The antitumor activity of 200 mg/kg Art was similar to that of 3 mg/kg cisplatin. In conclusion, Art exerted concentrationdependent inhibitory activity against esophageal cancer in vivo and in vitro by inducing cell apoptosis and cell cycle arrest through affecting mitochondrial membrane potential, BCL2, Bax, caspase3 and CDC25A.