Effect of phytochemicals on growth and prostaglandin E2 (PGE2) synthesis in PC-3 cells, a prostate cancer cell line
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The objectives of this thesis project was to identify the effects of phytochemicals commonly found in the diet on the growth of human prostate cancer PC-3 cells and determine the possible mechanisms by which these phytochemicals inhibit cell growth. These mechanisms include apoptosis, cell cycle progression, prostaglandin synthesis and the production of reactive oxygen species (ROS). PC-3 cells were initially supplemented with varying concentrations of resveratrol, β-sitosterol, omega-3 fatty acids, and vitamin E derivatives and cell growth was measured for up to 5 days. It was concluded from the initial screening that resveratrol and β-sitosterol had the greatest effect on inhibiting cell growth and further study was undertaken to determine the possible mechanism by which these phytochemicals exert their effect. Supplementation with resveratrol and β-sitosterol caused an increase in basal prostaglandin release with β-sitosterol having a greater effect. β-sitosterol was more effective than resveratrol in inducing apoptosis and the combination of the two had an intermediate effect. Cells supplemented with β-sitosterol were arrested at the G 2 /M phase and at the G 1 phase in the case of resveratrol while the combination resulted in cell arrest at the two phases of the cell cycle. β-sitosterol increased ROS production while resveratrol decreased ROS production. The combination of the two phytochemicals resulted in an intermediate effect. The observed changes in ROS and prostaglandin levels by these two phytochemicals may suggest the mechanism of action by which they inhibit cell growth. It was concluded that these two phytochemicals may induce the inhibition of the tumor growth by stimulating apoptosis and arresting cell growth at different locations in the cell cycle and the mechanism of action may involve modifications in ROS and prostaglandin production.