Expression profiles of E-cadherin and N-cadherin in endometriosis and other gynecological diseases towards targeted treatment: a systematic review

review OA: diamond CC0

Abstract

This systematic review aimed to summarize all available data and evaluate the roles of E-cadherin, N-cadherin, associated molecules, and signaling pathways in the pathogenesis of endometriosis. The search was conducted on PubMed, Cochrane Library, ClinicalTrials.gov, Scopus, Embase, and Google Scholar electronic databases. Twenty-two studies were included in the qualitative analyses. Several studies reported reduced E-cadherin expression in the ectopic and eutopic endometrium of patients with endometriosis, compared with that in the endometrium of patients without endometriosis (healthy comparison group and patients with non-malignant gynecological diseases). Moreover, some of the included studies reported higher E-cadherin concentration in endometriotic lesions than in the eutopic endometrium of patients with endometriosis. Similar results were obtained for β-catenin concentration. Some studies found that the expression levels of N-cadherin, ZEB1, ZEB2, TWIST, vimentin, SNAIL, SLUG, matrix metalloproteinases-9, and hypoxia-inducible factor-1α were higher in patients with endometriosis and that the E-cadherin levels were lower in ovarian and endometrial carcinomas than in endometriosis. These findings support the transplantation theory of endometriosis pathogenesis and highlight the potential therapeutic value of modulating E-cadherin and N-cadherin expression. Further research should be conducted to explore targeted treatment strategies for endometriosis.

My notes (saved in your browser only)

Condition tags

endometriosis

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.

References (75)

Source provenance

europepmc
last seen: 2026-06-04T01:30:01.192114+00:00
openalex
last seen: 2026-06-10T17:14:06.276822+00:00
pmc
last seen: 2026-05-13T20:22:03.195721+00:00
pubmed
last seen: 2026-05-16T00:31:04.451993+00:00
License: CC0 · commercial use OK