Abstract
Adipose-derived stem cell exosomes (ADSCs-Exos) enhance endometrial carcinoma (EC) cell proliferation, migration, and invasion. Mechanistically, ADSCs-Exos downregulate MAGED4B and CDH1, reduce E-cadherin expression, and upregulate vimentin, promoting epithelial-mesenchymal transition (EMT). Overexpression of MAGED4B reverses these effects and inhibits malignant behaviors. Furthermore, ADSCs-Exos increase organoid viability and confirm key protein changes. These findings demonstrate that ADSCs-Exos promote EC progression via the MAGED4B/CDH1/EMT axis.