Duo Liu1, Na Yang2, Yanchun Liang1, Ming Chen1, Fan Yang1, Lin Liu3, Shuzhong Yao1. 1. Department of Obstetrics and Gynecology, First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, China. 2. Department of Operating Room, First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, China. 3. Department of Clinical Research, Yangtze River Pharmaceutical Group, Taizhou, China.
Abstract
AIM: To study the involvement and interrelationship of epithelial cell adhesion molecule (EpCAM) and epithelial-mesenchymal transition (EMT) in endometriosis. METHODS: Samples from 114 patients undergoing endometrial biopsy or operation for endometriosis and 23 premenopausal women undergoing endometrial biopsy for non-endometriotic benign disease. Immunohistochemistry was used to detect expression level of EpCAM, E-cadherin and N-cadherin in endometrium from patients with (n = 24) and without endometriosis (n = 23), and in lesions from bowel (n = 46), peritoneal (n = 20) and ovarian (n = 24) endometriosis. RESULTS: There was no significant difference in the expression level of EpCAM, E-cadherin and N-cadherin, respectively, between endometrium from women with and without endometriosis (P > 0.05). There was also no significant difference in the expression level of EpCAM, E-cadherin and N-cadherin, respectively, among lesions from the bowel, peritoneal and ovarian endometriosis (P > 0.05). We found that the immunoreactivity of endometriotic epithelial cells to EpCAM and N-cadherin was significantly higher than that of eutopic endometrium, but decreased to E-cadherin (P < 0.05). According to the expression level of EpCAM, the expression level of E-Cadherin was significantly lower in endometriotic lesions with EpCAM expression above the mean level compared with that of endometriotic lesions with EpCAM expression below mean level, while the expression level of N-cadherin was contrary (P < 0.001). EpCAM staining level was negatively correlated with E-cadherin but positively correlated with N-cadherin (P < 0.001). CONCLUSIONS: These data suggest that overexpression of EpCAM, accompanied by an EMT, might be involved in endometriosis. EMT may be induced by the overexpression of EpCAM, thus promoting the development of endometriosis, which needs future studies to confirm for the pathogenesis of endometriosis.
AIM: To study the involvement and interrelationship of epithelial cell adhesion molecule (EpCAM) and epithelial-mesenchymal transition (EMT) in endometriosis. METHODS: Samples from 114 patients undergoing endometrial biopsy or operation for endometriosis and 23 premenopausal women undergoing endometrial biopsy for non-endometriotic benign disease. Immunohistochemistry was used to detect expression level of EpCAM, E-cadherin and N-cadherin in endometrium from patients with (n = 24) and without endometriosis (n = 23), and in lesions from bowel (n = 46), peritoneal (n = 20) and ovarian (n = 24) endometriosis. RESULTS: There was no significant difference in the expression level of EpCAM, E-cadherin and N-cadherin, respectively, between endometrium from women with and without endometriosis (P > 0.05). There was also no significant difference in the expression level of EpCAM, E-cadherin and N-cadherin, respectively, among lesions from the bowel, peritoneal and ovarian endometriosis (P > 0.05). We found that the immunoreactivity of endometriotic epithelial cells to EpCAM and N-cadherin was significantly higher than that of eutopic endometrium, but decreased to E-cadherin (P < 0.05). According to the expression level of EpCAM, the expression level of E-Cadherin was significantly lower in endometriotic lesions with EpCAM expression above the mean level compared with that of endometriotic lesions with EpCAM expression below mean level, while the expression level of N-cadherin was contrary (P < 0.001). EpCAM staining level was negatively correlated with E-cadherin but positively correlated with N-cadherin (P < 0.001). CONCLUSIONS: These data suggest that overexpression of EpCAM, accompanied by an EMT, might be involved in endometriosis. EMT may be induced by the overexpression of EpCAM, thus promoting the development of endometriosis, which needs future studies to confirm for the pathogenesis of endometriosis.