EDIL3 promotes apoptosis resistance through an integrin αvβ5-KLF2-CDC20 axis in endometriosis

Deyu Zhang, Jingwen Zhu, Peili Wu, Yan Huang, Xiaorong Wang, Chao Peng, Yingfang Zhou, Qing Xue
In: Current Molecular Pharmacology · 2026 · doi:10.1016/j.cmp.2026.09.004 · W7213400805
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EDIL3 promotes apoptosis resistance in endometriosis through an integrin αvβ5-KLF2-CDC20 axis.

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Abstract

Background Apoptosis resistance promotes the persistence of ectopic endometrial cells, but its extracellular regulators remain incompletely understood. This study aimed to determine whether EDIL3 promotes stromal-cell survival in endometriosis and to investigate the associated signaling pathway. Methods Transcriptomic screening combining weighted gene co-expression network analysis with secreted-protein annotation was used to identify lesion-associated candidates. EDIL3 was examined in plasma, paired tissues, public single-cell datasets, primary stromal cells, functional experiments, RNA sequencing, co-immunoprecipitation, ChIP-qPCR, and a syngeneic mouse model. Results EDIL3 was upregulated in ectopic lesions and lesion-derived stromal cells. Among 92 patients and 80 controls, plasma EDIL3 yielded an area under the curve of 0.790, with 77.2% sensitivity and 71.3% specificity at 12.41 ng/mL. EDIL3 silencing increased apoptosis and reduced proliferation, whereas overexpression produced opposite effects. KLF2 overexpression partially rescued EDIL3-silenced cells. EDIL3-associated complexes contained ITGAV and ITGB5, and their simultaneous knockdown attenuated EDIL3-induced KLF2 expression. KLF2 regulated CDC20 expression and occupied a motif-containing CDC20 promoter region. CDC20 gain- and loss-of-function supported its involvement in apoptosis. In mice, EDIL3 knockdown reduced ectopic lesion growth, which KLF2 overexpression partially reversed. Conclusions EDIL3 regulates ectopic stromal cell survival in endometriosis, at least in part, through a proposed integrin αvβ5-KLF2-CDC20 axis. The potential diagnostic and therapeutic relevance of EDIL3 requires further validation.

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