Niclosamide Suppresses Proliferation, Induces Apoptosis and Inhibits Wnt/beta-catenin Signaling Pathway in Human Ovarian Cancer Cells

Abstract

Objective: The aim of this study is to investigate in vitro effects of an antihelminthic drug niclosamide on human ovarian carcinoma cell line OVCAR3. Methods: MTT assay was applied to investigate the cytotoxic effects of niclosamide on the cells. beta-catenin levels in the cells were analyzed by immunocytochemistry, in order to assess the potency of niclosamide on Wnt/beta-catenin signaling pathway that function in cell proliferation. The effects of the drug on apoptosis were detected by TUNEL method. All the assays were also performed for chemotherapy agent 5-fluorouracil (5-FU) and anticancer effects of these two drugs were compared. Results: It was found that niclosamide at 1 mu M and 2 mu M concentrations reduced cell viability, whereas 5-FU showed its significant proliferation inhibitory effect at higher concentrations. Niclosamide led to an increase in apoptosis while this effect was weaker compared with 5-FU. Niclosamide treatment decreased beta-catenin staining in the cells significantly but 5-FU did not affect beta-catenin levels. Conclusion: The results indicate that niclosamide induces apoptosis and suppresses cell proliferation by inhibiting Wnt/beta-catenin signaling pathway in OVCAR-3 cells. In conclusion, these findings warrant further evaluation of niclosamide as a promising therapy for ovarian cancer.