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Tropical Journal of Pharmaceutical Research
Pharmacotherapy Group, Faculty of Pharmacy, University of Benin, Benin City, Nigeria
ISSN: 1596-5996 EISSN: 1596-5996
Vol. 16, No. 4, 2017, pp. 781-785
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Bioline Code: pr17099
Full paper language: English
Document type: Research Article
Document available free of charge
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Tropical Journal of Pharmaceutical Research, Vol. 16, No. 4, 2017, pp. 781-785
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Emodin inhibits proliferation and invasion, and induces apoptosis in human esophageal cancer cell line ECA109
Zhao, Chuan; Wu, Youyi; Li, Fuyao & Jin, Xiaosheng
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
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