Purpose: To determine the anticancer effects of emodin in human esophageal carcinoma cell line ECA109. Methods: Cell viability was determined by MTT assay, while cell invasion and apoptosis were measured by Transwell assay and flow cytometry, respectively. Expression levels of MMP-2, Bax, Bcl-2 and caspase-3 proteins were determined by Western blot. Results: Flow cytometry data showed that the proportion of apoptotic cells was increased by emodin treatment. Apoptotic rates produced by 10, 20

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... 50 μM emodin were 13.9 ± 3.8, 25.6 ± 6.2 and 39.8 ± 7.7 %, respectively. Transwell assay data revealed concentration-dependent suppression of the invasive rate of ECA109 cells by emodin (10, 20 and 50 μM) was 30.0 ± 4.5, 56.0 ± 6.8 and 69.0 ± 8.1 %, respectively. Furthermore, emodin treatment inhibited expressions of MMP-2 and Bcl-2 proteins, but induced the expression of Bax and caspase-3, when compared with control groups. Conclusion: These results suggest that emodin inhibits cell proliferation and cell invasion, but induces cell apoptosis in human esophageal cancer cell line ECA109. Thus, emodin is a potential candidate for development of an effective chemotherapeutic agent against esophageal cancer.