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  • Title: Caffeic acid phenethyl ester induces apoptosis of human pancreatic cancer cells involving caspase and mitochondrial dysfunction.
    Author: Chen MJ, Chang WH, Lin CC, Liu CY, Wang TE, Chu CH, Shih SC, Chen YJ.
    Journal: Pancreatology; 2008; 8(6):566-76. PubMed ID: 18824880.
    Abstract:
    AIMS: This study aimed to investigate the effect of caffeic acid phenethyl ester (CAPE), an active component isolated from honeybee propolis, in inducing apoptosis in human pancreatic cancer cells. METHODS: Inhibition of viability of BxPC-3 and PANC-1 cell lines induced by CAPE was estimated by a trypan blue dye exclusion test. The type of cell death in BxPC-3 after CAPE treatment was characterized by observation of morphology, sub-G1 DNA content, annexin-V/PI staining, caspase-3 and caspase-7 assay, and DNA agarose gel electrophoresis. RESULTS: CAPE (10 microg/ml) resulted in marked inhibition of viability of BxPC-3 (80.4 +/- 4.1%) and PANC-1 (74.3 +/- 2.9%) cells. CAPE induced a time-dependent increase in hypodiploid percentage and a significant decrease in mitochondrial transmembrane potential in BxPC-3 cells. It induced morphological changes of typical apoptosis, but no DNA fragmentation was noted by DNA electrophoresis. The inhibition of growth and increased in the proportion of sub-G(1) cells was partially blocked by pretreatment with the pan-caspase inhibitor Z-VAD-fmk (50 microM) in BxPC-3 cells indicating a caspase-related mechanism in CAPE-induced apoptosis. Caspase-3/caspase-7 activity was approximately 2 times greater in CAPE-treated BxPC-3 cells compared with control cells. CONCLUSIONS: These results suggest that CAPE is a potent apoptosis-inducing agent. Its action is accompanied by mitochondrial dysfunction and activation of caspase-3/caspase-7.
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