The aim of the present study was to investigate licochalcone-E (Lico-E)-induced 
apoptosis and the associated apoptotic signaling pathway in FaDu cells, a human 
pharyngeal squamous carcinoma cell line. Treatment with Lico-E exhibited 
significant cytotoxicity on FaDu cells in a concentration-dependent manner. The 
IC50 value of Lico-E in FaDu cells was ~50 µM. Treatment with Lico-E increased 
the number of dead FaDu cells. Furthermore, chromatin condensation, which is 
associated with apoptotic cell death, was observed in FaDu cells treated with 
Lico-E for 24 h. By contrast, Lico-E did not produce cytotoxicity or increase 
the number of dead cells when applied to human normal oral keratinocytes 
(hNOKs). Furthermore, chromatin condensation was not observed in hNOKs treated 
with Lico-E. Treatment with Lico-E increased the expression of Fas ligand and 
the cleaved form of caspase-8 in FaDu cells. Furthermore, treatment with Lico-E 
increased the expression of pro-apoptotic factors, including apoptosis regulator 
BAX, Bcl-2-associated agonist of cell death, apoptotic protease-activating 
factor 1, caspase-9 and tumor suppressor p53, while decreasing the expression of 
anti-apoptotic factors, including apoptosis regulator Bcl-2 and Bcl-2-like 
protein 1 in FaDu cells. The expression of cleaved caspases-3 and poly 
(ADP-ribose) polymerase was significantly upregulated following treatment with 
Lico-E in FaDu cells, while Lico-E-induced apoptotic FaDu cell death was 
partially suppressed by treatment with Z-VAD-FMK, a pan caspase inhibitor. 
Therefore, Lico-E-induced oral cancer (OC) cell-specific apoptosis is mediated 
by the death receptor-dependent extrinsic and mitochondrial-dependent intrinsic 
apoptotic signaling pathways. In conclusion, these data suggested that Lico-E 
exhibits potential chemopreventive effects and warrants further developed as a 
chemotherapeutic agent against OC.