Correlation between Polycomb repressive complex proteins and epithelial-mesenchymal transition-associated genes in endometriotic tissues.

Endometriosis is a condition in which functional endometrial glands and stroma are found to grow outside the uterine cavity that can lead to symptoms like dysmenorrhea, dyspareunia, adhesions, and infertility. Current treatment strategies can provide only symptomatic relief as its etiology remains unclear. Several studies have linked the cellular process of epithelial-mesenchymal transition (EMT) to endometriosis development; however, what triggers EMT states in endometriosis is unknown. Polycomb group (PcG) proteins are histone modifiers that control gene expression by catalyzing repressive histone modifications such as H3K27me3/2 and H2AK119ub1. The misexpression of PcGs and/or genes controlled by them reportedly causes several types of cancers, such as breast, colon, pancreatic, and liver. We investigated whether dysregulation of PcG proteins such as RING1B, BMI1, and EZH2 in ectopic endometriotic tissue as compared to eutopic correlates with genes required for EMT in endometriotic tissue from the same patient with laparoscopically confirmed endometriosis. We quantified the expression of Polycomb repressive complex 1 (PRC1) genes (RING1B and BMI1), EMT-associated genes (TWIST, SNAI1, SNAI2, ZEB1, CDH1, CDH2, and VIM) in paired eutopic and ectopic (endometriotic) tissue samples obtained from 12 women who underwent laparoscopy for severe endometriosis identified as per #ENZIAN classification. Our results showed that the endometriotic lesions had higher gene expression of PRC1 proteins - RING1B and BMI1 as well as higher expression of EMT associated genes than the endometrial tissue. Thus, our results suggest that PRC1 proteins may have a role in the pathogenesis of endometriosis.