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The percentage viability of HeLa cells significantly deceased after treatment with WBCex in a dose\u2010 and time\u2010dependent manner. The IC<jats:sub>50<\/jats:sub> dose was suggested to be approximately 225 \u03bcg\/mL protein. Apoptotic cell death occurred in a time\u2010dependent manner based on investigation by flow cytometry using annexin V\u2010FITC and PI staining. DAPI nucleic acid staining indicated increased chromatin condensation. Caspase\u20103, \u22128 and \u22129 activities also increased, suggesting the induction of the caspase\u2010dependent apoptotic pathway. Furthermore, the mitochondrial membrane potential (\u0394\u03a8<jats:sub>m<\/jats:sub>) of HeLa cells was lost as a result of increasing levels of Bax and reduced levels of Bcl\u20102, Bcl\u2010XL, Bcl\u2010Xs, and XIAP. The decreased \u0394\u03a8<jats:sub>m<\/jats:sub> led to the release of cytochrome <jats:italic>c<\/jats:italic> and the activation of caspase\u20109 and \u22123. Apoptosis\u2010inducing factor translocated into the nuclei, and endonuclease G (Endo G) was released from the mitochondria. These results suggest that anticancer agents in WBCex can induce apoptosis in HeLa cells via both caspase\u2010dependent and \u2010independent pathways. \u00a9 2015 Wiley Periodicals, Inc. 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