The role of the adhesion molecule Nectin-4 in the pathogenesis of endometriosis
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Abstract
OBJECTIVE: Nectins are immunoglobulin-like adhesion molecules, and they play important role in cell proliferation and tumor metastasis. The objective in this study was to compare the expression of Nectin-4 in normal endometrium and in ectopic endometriotic tissues. MATERIALS AND METHODS: Nectin-4 expression was investigated in ovarian endometriosis (n = 20), peritoneal endometriosis (n = 20), endometrium of endometriosis (n = 20), and in a control group (having no endometriosis) (n = 20) by immunohistochemical method. RESULTS: Nectin-4 expression, when compared with control group, was higher in endometriotic lesions of patients having ovarian endometriosis and peritoneal endometriosis (p = 0.003 and p = 0.009, respectively). This difference was significant in the endometrium of patients having endometriosis (p = 0.011). CONCLUSION: The authors believe that Nectin-4 molecule may contribute to the pathogenesis of endometriosis. For this reason, the use of medicines developed against this molecule in the treatment of endometriosis may be useful.
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Cited by (8)
- The Role of Cadherin 12 (CDH12) in the Peritoneal Fluid among Patients with Endometriosis and Endometriosis-Related Infertility 2022
- Ectopic Endometrial Cell-Derived Exosomal Moesin Induces Eutopic Endometrial Cell Migration, Enhances Angiogenesis and Cytosolic Inflammation in Lesions Contributes to Endometriosis Progression 2022
- A Comparative Study of Endometriosis and Normal Endometrium Based on Ultrasound Observation 2022
- Macrophage-derived netrin-1 contributes to endometriosis- associated pain 2021
- Exosomal Moesin Derives From Ectopic Stromal Cells Constructs A “Migration-Vascularization-Inflammation” Loop In Endometriosis 2021
- Macrophage-derived Netrin-1 participates in endometriosis-associated pain 2019
- Transforming growth factor β1 enhances adhesion of endometrial cells to mesothelium by regulating integrin expression 2017
- 10.1016/s0246-1064(17)65070-9 2000
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