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Trichostatin A (TSA) as a HDAC inhibitor can regulate many biological propertiesincluding apoptosis and cell proliferation in various cancer cells. Here, we evaluatedthe effect of TSA on the growth and death of HeLa cervical cancer cells in relationto reactive oxygen species (ROS) and glutathione (GSH) levels. Dose- and time-dependentgrowth inhibition was observed in HeLa cells with an IC50 of approximately 20nM at 72 h. This agent also induced apoptotic cell death, as evidenced by annexinV-FITC staining cells, caspase-3 activation and the loss of mitochondrial membranepotential (MMP; ∆ψm). In addition, the administration of Bcl-2 siRNA intensifiedTSA-induced HeLa cell death. All of the tested caspase inhibitors significantlyrescued some cells from TSA-induced HeLa cell death. TSA increased O2•- leveland induced GSH depletion in HeLa cells. Caspase inhibitors significantly attenuatedO2•- level and GSH depletion in TSA-treated HeLa cells. In addition, N-acetylcysteine (NAC; a well known antioxidant) significantly prevented cell death andGSH depletion in TSA-treated HeLa cells via decreasing O2•- level. In conclusion,TSA inhibited the growth of HeLa cells via Bcl-2-mediated apoptosis, which wasclosely related to O2•- and GSH content levels.

Trichostatin A induces apoptotic cell death of HeLa cells in a Bcl-2 and oxidative stress-dependent manner