Diosgenin Induces Apoptosis of MCF-7 Cells by Regulating DAXX Subcellular Localization and Activating JNK/p38 Signaling Pathway

Objective To investigate the effect of diosgenin on proliferation and apoptosis of breast cancer cells and its potential molecular mechanism. Methods The breast cancer cell line MCF-7 was treated with low, medium and high doses of diosgenin, the cell proliferation was detected by MMT method. Flow cytometry was used to detect cell apoptosis. Nuclear cytoplasmic protein separation method and immunofluorescence were applied to detect the subcellular localization of death associated protein (DAXX). qRT-PCR and western blot were used to detect the expression of DAXX and c-Jun N-terminal kinase pathway (JNK) related protein. Results diosgenin significantly inhibit the proliferation of MCF-7 cells and promote their apoptosis with concentration dependence. Diosgenin promoted DAXX moving from nucleus into cytoplasm, upregulated the expression of cell surface death receptor (Fas), increased the phosphorylation levels of JNK and mitogen activated protein kinase (p38), and activated the JNK/p38 signaling pathway. Conclusion Diosgenin inhibits the proliferation and apoptosis of breast cancer cell line MCF-7, whose mechanism might be related to the regulation of DAXX subcellular localization and the activation of JNK/p38 signaling pathway.