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We demonstrated that GHSC\u201074 reduced the viability of HepG2 cells in a time\u2010 and dose\u2010dependent manner, and efficiently induced apoptosis without significantly decreasing the viability of Chang human liver cells and Swiss albino 3T3 fibroblasts, as indicated by annexin\u2010V\/PI binding assay and Hoechst 33342 staining. In addition, stimulation of HepG2 cells with GHSC\u201074 induced a series of intracellular events: (1) loss of mitochondrial membrane potential; (2) sustained elevation of cytosolic [Ca<jats:sup>2+<\/jats:sup>]; and (3) downregulation of Bcl\u20102. BAPTA\u2010AM, a cytosolic Ca<jats:sup>2+<\/jats:sup> chelator, partly suppressed cell death and prevented mitochondrial membrane potential from losing in GHSC\u201074\u2010treated HepG2 cells. In contrast, EGTA, an extracellular Ca<jats:sup>2+<\/jats:sup> chelator, exhibited a weaker effect as compared to that of BAPTA\u2010AM. 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