P-219: The Role of E-Cadherin Coding Gene (CDH1) in Pathogenesis of Endometriosis

Background: Endometriosis, a gyncological disorder,benign and common cause of infertility, is defined as the presence of endometrial glands and stroma at ectopic locations outside the uterine cavity. Clinical observations have led to the assessment that endometriosis is an invasive disease. Abnormal expression of adhesion molecules such as cadherins is likely to be an important determinant of local invasion and dissemination. Cadherins are major cell-cell adhesion molecules involved in the development and maintenance of all solid tissues. E-cadherin is a transmembrane glycoprotein and a member of the multigene superfamily of cadherins and it is a crucial adhesion molecule which hampers tumor invasion and metastasis. In the current work, the expression of E-cadherin gene (CDH1) has been evaluated in eutopic and ectopic endometrium of women with endometriosis. Materials and Methods: Local ethical approval was gained for this study and informed consent was given by patients. The levels of CDH1 gene expression in ectopic and eutopic endometrium in women with endometriosis were investigated and compared with the endometrium samples of women without endometriosis. Ectopic biopsies were obtained by laparoscopic procedure and eutopic biopsies were obtained by piplle. In women without endometriosis, control biopsies were gained with piplle. Quantitative PCR was performed on cDNA samples using CDH1 primers, and GAPDH was used as housekeeping gene. Results: This study showed that CDH1 gene expression in eutopic and ectopic endometrium was significantly lower than normal endometrium. On the other side, mRNA level of CDH1 was significantly higher in eutopic endometrium compared to ectopic endometrium. Conclusion: These findings suggest that CDH1 gene could be involved in pathogenesis of endometriosis, in the way that decrease of CDH1 gene expression could lead to invasiveness and metastasis in patients with endometriosis.