Journal
ANTI-CANCER AGENTS IN MEDICINAL CHEMISTRY
Volume 17, Issue 11, Pages 1570-1577Publisher
BENTHAM SCIENCE PUBL LTD
DOI: 10.2174/1871520617666170327155930
Keywords
Citalopram; cancer; apoptosis; Bay11-7082; cytotoxicity; HepG2
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Funding
- Drug Applied Research Center of Tabriz University of Medical Sciences, Tabriz, Iran [77/93]
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Background: Evidence has been provided of the anti-proliferative activity of citalopram against some cancer cells. Objective: The apoptotic impact of citalopram, an antidepressant, against liver hepatocellular carcinoma cell line HepG2 was investigated in relation to the oxidative pathway and nuclear factor (NF)kappa B activation. Method: The cytotoxic effects of citalopram on HepG2 cells were determined by MTT assay. Reactive oxygen species (ROS) formation and cytochrome c release were measured following treatment with citalopram. Apoptosis analysis and Bax and Bcl-2 mRNA and protein levels were also determined. Results: The cytotoxic effects of different concentrations of citalopram on HepG2 cells were observed as a reduction in cell viability and an increase in ROS formation. Citalopram caused an increase in mitochondrial Bax levels and a decrease in Bcl2 levels and also caused cytochrome c release. Moreover, DAPI staining and flow cytometry assays revealed citalopram-induced apoptosis in HepG2 cells. Oxidant scavengers and Bay 11-7082 (an irreversible inhibitor of NF kappa B activation) prevented the citalopram-associated cell death, increased BAX and decreased Bcl2. Conclusion: Outcomes from current study suggest that citalopram might exhibit apoptotic effect against hepatocellular carcinoma cell line by induction of cell death through cytochrome c release and ROS-dependent activation of NF kappa B.
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