Chalcones are precursors of
flavonoids that exhibit structural heterogeneity and potential antitumor activity. The objective of this study was to characterize the cytotoxicity of trans-
chalcone and
licochalcone A (LicoA1) against a
breast cancer cell line (MCF-7) and normal murine fibroblasts (3T3). Also the mechanisms of the anti-
cancer activity of these two compounds were studied. The alkaline comet assay revealed dose-dependent genotoxicity, which was more responsive against the tumor cell line, compared to the 3T3 mouse fibroblast cell line. Flow cytometry showed that the two
chalcones caused the cell cycle arrest in the G1 phase and induced apoptosis in MCF-7 cells. Using PCR Array, we found that trans-
chalcone and LicoA trigger apoptosis mediated by the intrinsic pathway as demonstrated by the inhibition of Bcl-2 and induction of Bax. In western blot assay, the two
chalcones reduced the expression of cell death-related
proteins such as Bcl-2 and
cyclin D1 and promoted the cleavage of PARP. However, only trans-
chalcone induced the expression of the CIDEA gene and
protein in these two experiments. Furthermore, transient transfections of MCF-7 using a construction of a promoter-
luciferase vector showed that trans-
chalcone induced the expression of the CIDEA promoter activity in 24 and 48h. In conclusion, the results showed that trans-
chalcone promoted high induction of the CIDEA promoter gene and
protein, which is related to DNA fragmentation during apoptosis.