Introduction: Up-regulation of phospholipase D (PLD) is functionally related to tumorigenesis and oncogenic signals. Chrysin, caffeic acid phenethyl ester (CAPE) and ethanolic extract of propolis (EEP) are three safe compounds which have been shown to possess antiproliferative, antioxidant, anti-inflammatory and antineoplastic properties. In this study, the effects of these three compounds on PLD1 gene expression were examined in AGS cell line. Methods: After determining the appropriate concentrations of EEP, CAPE, and chrysin, AGS cells were cultured in mediums with proper ratios of the compounds. AGS cells were maintained in exponential growth and the culture mediums refreshed every other day. Finally, after extracting total RNA from AGS cells, real-time PCR was performed to evaluate the mRNA expression of PLD1 in the presence of each compound. Results: CAPE decreased the mRNA level of PLD1 gene in a dose-dependent manner. A solution with 30 μM concentration of CAPE was the effective dose in comparison to control group as well as 15 and 20 μM concentrations of the compound, whereas no changes were observed in the presence of EEP and chrysin. Conclusion: Taken together, the results of the study indicated that CAPE might exert its anti-neoplastic effect by targeting PLD1 expression in AGS cell line.

Background: Propolis is a natural product of bee and caffeic acid phenethyl ester (CAPE) is a pharmacologically important product of propolis. Objectives: The aim of this study was to investigate the effect of CAPE on apoptosis induction in AGS human gastric cancer cells. Materials and Methods:The cytotoxic effects of CAPE at different concentrations were investigated on AGS cells viability after 24 hours treatment by MTT assay. To measure the effect of CAPE on apoptosis induction, AGS cells were treated with CAPE for 24 hours and investigated by FITC Annexin V/PI staining using flow cytometry. Results: CAPE prevented growth and proliferation of AGS human gastric cancer cell line in a concentration-dependent manner with an IC50 of approximately 60 µM by a 24-hour treatment. Also CAPE caused increased induction of apoptosis in AGS cells from 1.37 % in control cells to 21.76 % in treated cells with 30 µM CAPE. Conclusions: CAPE prevents growth and proliferation of AGS human gastric cancer cell line through inducing programmed cell death in AGS cells. Therefore, CAPE could be helpful for developing chemotherapeutic agents or as an adjuvant for human gastric cancer treatment.