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