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.