Endometriosis is a benign, estrogen-dependent gynecological condition with an uncertain exact pathogenetic mechanism. The aim of this study was to evaluate the potential differential expression of Insulin Growth Factor 1 (IGF-1) isoforms in deeply infiltrating endometriotic (DIE) lesions, in ovarian endometriomas, and in the eutopic endometrium of the same endometriosis patients and to compare their expression with that in the eutopic endometrium of women without endometriosis. A total of 39 patients were included: 28 with endometriosis, of whom 15 had endometriomas only, 7 had DIE nodules only, and 6 had both DIE and endometriomas, and 11 without endometriosis served as controls. We noticed a similar pattern of expression between IGF-1Ea and IGF-1Ec, which differed from that of the IGF-1Eb isoform, possibly implying differential biological actions of different isoforms in DIE subtypes. We observed a tendency of lower expression of IGF-1Ea and IGF-1Ec in endometriomas without DIE compared to endometriomas with concurrent DIE or in DIE nodules. In conclusion, differential expression of IGF-1 isoforms may indicate that DIE with its associated ovarian lesions and simple ovarian endometriosis should be considered as two forms of the disease developing under different molecular pathways.

Background/Objectives: Epithelial–Mesenchymal Transition (EMT) is the process by which epithelial cells acquire mesenchymal properties, which helps endometriotic cells migrate and invade. This study looks at the expression of E-CADHERIN, a critical epithelial marker, and miR-200b, an EMT regulator, in several types of endometriosis, including endometriomas and deep infiltrating endometriotic (DIE) nodules. Methods: We examined 19 individuals with endometriosis (9 with just endometriotic cysts and 10 with both DIE and endometriotic cysts) and 8 controls with benign gynecological abnormalities. Tissue samples were taken during laparoscopic surgery, and E-CADHERIN and miR-200b expression were measured using Real-Time PCR, with G6PD and U6 as controls. Results:E-CADHERIN expression was maintained in the eutopic endometrium of both ovarian and DIE types, but it was considerably reduced in endometriotic cysts, indicating heightened mesenchymal features. miR-200b was downregulated in the eutopic endometrium of ovarian endometriosis but upregulated in DIE. Endometriotic cysts in both groups had greater miR-200b expression than their corresponding eutopic endometrium. E-CADHERIN and miR-200b expression in DIE lesions was similar to that found in matched eutopic endometrium. Conclusions: The regulation of E-CADHERIN and miR-200b varies across ovarian and DIE lesions. The miR-200b-ZEB1 feedback loop is increased in DIE eutopic endometrium but downregulated in ovarian endometriosis. E-CADHERIN downregulation in endometriotic cysts indicates heightened mesenchymal dynamics, whereas DIE nodules have gene expression patterns similar to eutopic endometrium. These findings emphasize the distinct regulatory processes that govern endometriotic lesions.