Tropical Journal of Pharmaceutical Research

Original Research Article | OPEN ACCESS

Emodin inhibits proliferation and invasion, and induces apoptosis in human esophageal cancer cell line ECA109

Chuan Zhao¹, Youyi Wu², Fuyao Li², Xiaosheng Jin³

¹Department of Pharmacy, Navy General Hospital PLA China, Beijing, 100048; ²Department of Medical Oncology; ³Department Digestive Medicine, Ruian People’s Hospital, Ruian, Zhejiang, PR China, 325200.

For correspondence:- Xiaosheng Jin Email: jinxsheng@126.com

Received: 24 November 2016 Accepted: 14 March 2017 Published: 29 April 2017

Citation: Zhao C, Wu Y, Li F, Jin X. Emodin inhibits proliferation and invasion, and induces apoptosis in human esophageal cancer cell line ECA109. Trop J Pharm Res 2017; 16(4):781-785 doi: 10.4314/tjpr.v16i4.6

© 2017 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..

Abstract

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 and 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

Keywords: Emodin, Esophageal Cancer, Apoptosis, Cell invasion, Bax, Caspase-3