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

• Published in: Zhongliu fangzhi yanjiu Vol. 52; no. 5; pp. 368 - 373
• Main Authors: Wang, Jia, Gao, Shilei, Zhang, Lihan, Zhang, Lu, Sun, Xu, Li, Huahua, Liu, Huaimin
• Format: Journal Article
• Language: Chinese; English
• Published: Tianjin China Anti-Cancer Association 2025; Magazine House of Cancer Research on Prevention and Treatment
• Subjects: Apoptosis; Breast cancer; c-Jun protein; Cell death; Cell proliferation; Cell surface; Cytoplasm; daxx; Daxx protein; diosgenin; Flow cytometry; JNK protein; jnk/p38 signaling pathway; Kinases; Localization; Molecular modelling; Phosphorylation; Protein purification; Proteins; Signal transduction; Transcription factors
• ISSN: 1000-8578
• DOI: 10.3971/j.issn.1000-8578.2025.24.0980

Objective To investigate the effect of diosgenin on the 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, and cell proliferation was detected through the MMT method. Flow cytometry was used to detect cell apoptosis. Nuclear-cytoplasmic-protein separation method was applied to detect the subcellular localization of death associated protein (DAXX). qRT-PCR and Western blot were used to detect the expressions of DAXX and c-Jun N-terminal kinase pathway (JNK)-related proteins. Results Diosgenin considerably inhibited the proliferation of MCF-7 cells and promoted cell apoptosis in a concentration-dependent manner. Diosgenin can promote the movement of DAXX from nucleus into the cytoplasm. Diosgenin 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 with concentration dependence. Conclusion Diosgenin inhibits the proliferation and promotes the apoptosis of the breast cancer cell line MCF-7, whose mechanism may be related to the regulation of DAXX subcellular localization and the activation of JNK/p38 signaling pathway.