Effect of fraxetin on proliferation and apoptosis in breast cancer cells

Abstract

The aim of the present study was to examine the effect of fraxetin on proliferation and apoptosis in the MCF-7 breast cancer cell line. Cell proliferation was measused using an MTT assay and 4',6-diamidino-2-phenylindole (DAPI) staining was used to determine shrinkage and condensation. RT-PCR was used to examine the expression of factor-associated suicide (Fas) and Fas ligand (FasL) mRNA, and western blot analysis was used to examine Bax and Bcl-2 protein. MTT showed that the proliferation of MCF-7 cells was significantly inhibited by fraxetin in a dose-dependent manner. Fraxetin also induced significant morphological changes of MCF-7 cells, suggestive of apoptosis, whereas DAPI staining showed that fraxetin caused cell shrinkage and chromatin condensation. RT-PCR showed that the expression of Fas and FasL mRNA was upregulated by fraxetin and the western blot analysis revealed that Bax was upregulated and Bcl-2 was downregulated. In conclusion, fraxetin can inhibit the proliferation of MCF-7 cells, induce apoptosis, upregulate Fas, FasL and Bax, and downregulate Bcl-2 to induce apoptosis. These results support the potential therapeutic role for fraxetin in breast cancer.