CXADR promote epithelial-mesenchymal transition in endometriosis by modulating AKT/GSK-3β signaling

Hang-Jing Tan, Zi-Heng Deng, Chun Zhang, Hong‐Wen Deng, Hong-Wen Deng, Hong‐Mei Xiao, Hong-Mei Xiao
Cell cycle (Georgetown, Tex.) · 2023 · vol. 22(21-22) , pp. 2436–2448 · doi:10.1080/15384101.2023.2296242 · PMID:38146657 · PMC10802198 · W4390231211
article OA: green CC0 ⤵ 2 in-corpus citations
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⚙ AI-generated summary by claude@2026-06, 2026-06-08 ⓘ

CXADR promotes epithelial-mesenchymal transition in endometriosis by stabilizing PHLPP2 and PTEN, thereby suppressing AKT/GSK-3β signaling and increasing SNAIL1 levels.

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Abstract

Endometriosis is a benign high prevalent disease exhibiting malignant features. However, the underlying pathogenesis and key molecules of endometriosis remain unclear. By integrating and analysis of existing expression profile datasets, we identified coxsackie and adenovirus receptor (CXADR), as a novel key gene in endometriosis. Based on the results of immunohistochemistry (IHC), we confirmed significant down-regulation of CXADR in ectopic endometrial tissues obtained from women with endometriosis compared with healthy controls. Further in vitro investigation indicated that CXADR regulated the stability and function of the phosphatases and AKT inhibitors PHLPP2 (pleckstrin homology domain and leucine-rich repeat protein phosphatase 2) and PTEN (phosphatase and tensin homolog). Loss of CXADR led to phosphorylation of AKT and glycogen synthase kinase-3β (GSK-3β), which resulted in stabilization of an epithelial-mesenchymal transition (EMT) factor, SNAIL1 (snail family transcriptional repressor 1). Therefore, EMT processs was induced, and the proliferation, migration and invasion of Ishikawa cells were enhanced. Over-expression of CXADR showed opposite effects. These findings suggest a previously undefined role of AKT/GSK-3β signaling axis in regulating EMT and reveal the involvement of a CXADR-induced EMT, in pathogenic progression of endometriosis.

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Condition tags

endometriosis

MeSH descriptors

Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Proto-Oncogene Proteins c-akt Proto-Oncogene Proteins c-akt Proto-Oncogene Proteins c-akt Proto-Oncogene Proteins c-akt Proto-Oncogene Proteins c-akt Proto-Oncogene Proteins c-akt Proto-Oncogene Proteins c-akt Cell Adhesion Molecules Cell Adhesion Molecules Cell Adhesion Molecules Cell Adhesion Molecules Cell Adhesion Molecules Cell Adhesion Molecules

Citation neighborhood

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

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