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

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

ObjectiveTo investigate the effect of diosgenin on the proliferation and apoptosis of breast cancer cells and its potential molecular mechanism. MethodsThe breast cancer cell line MCF-7 was treated with low, medium, and high doses of diosgenin, and cell proliferation was detected through the MMT met...

Full description

Saved in:
Bibliographic Details
Main Authors: Jia WANG, Shilei GAO, Lihan ZHANG, Lu ZHANG, Xu SUN, Huahua LI, Huaimin LIU
Format: Article
Language:zho
Published: Magazine House of Cancer Research on Prevention and Treatment 2025-05-01
Series:Zhongliu Fangzhi Yanjiu
Subjects:
breast cancer
diosgenin
daxx
jnk/p38 signaling pathway
Online Access:http://www.zlfzyj.com/cn/article/doi/10.3971/j.issn.1000-8578.2025.24.0980
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:ObjectiveTo investigate the effect of diosgenin on the proliferation and apoptosis of breast cancer cells and its potential molecular mechanism. MethodsThe 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. ResultsDiosgenin 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. ConclusionDiosgenin 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.
ISSN:1000-8578

Similar Items