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This study investigated the functional role of microRNA miR-218 in endometriosis using human endometriotic epithelial cell lines and primary stromal cells. The researchers found that upregulating miR-218 significantly reduced cell invasiveness and viability, while simultaneously causing a downregulation of its predicted targets, EGFR and decorin. These findings highlight a potential mechanism where miR-218 suppresses key drivers of disease progression, such as proliferation and matrix signaling, by inhibiting these specific proteins. This paper is centrally about endometriosis — specifically focusing on the molecular pathogenesis involving miR-218-mediated regulation of EGFR and decorin in ectopic endometrial tissue.
Abstract
Endometriosis is an estrogen-dependent disease characterized by ectopic growth of endometrium-like glands and stroma outside the uterus. It has a considerable impact on endometrial receptivity: it is estimated, that 6%-10% of women in general and 35%-50% of women with pelvic pain or infertility suffer from the disease. Noteably, the expression of numerous microRNAs is dysregulated in endometriosis. microRNAs are small non-coding RNAs which regulate gene expression at the posttranscriptional level. Here, we characterize the functional impact of one microRNA previously show to be dysragulated in endometriosis – miR-218 – using an in vitro system. Emplyoing the human endometriotic epithelial cell line 12Z, we are able to demonstrate that miR-218 upregulation via transient transfection of precursor molecules results in reduced invasiveness in matrigel invasion chamber and in reduced cell viability. qPCR analysis in 12Z cells, in the endometrial stroma cell line St-T1b, and in patient-derived primary endometrial stroma cells reveled a significant downregulation of two predicted targets of miR-218, the epidermal growth factor receptor EGFR, and the proteoglycan decorin. While EGFR expression has been shown to be upregulated in severe versus mild disease, decorin is known to be expressed in an estrogen-dependent manner in the endometrium. Current investiations are therefore focussing on a detailed analysis of the contribution of these factors to the miR-218-dependent phenotype, since decorin contributes to the pathogenesis of malignant and inflammatory diseases by influencing angiogenesis and matrix-dependent signalling via TGFbeta and by interferon gamma signalling during inflammation. Furthermore, EGFR is involved in the regulation of cell proliferation, invasiveness and epithelial-to-mesenchymal transition, rendering these two factors promising candidates for the miR-218-dependent pathogenetic mechanism.
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DOI: 10.1055/s-0035-1547731
Functional analysis of microrna miR-218 in endometriosis: Role of EGFR and the TGFbeta-binding proteoglycan decorin
Endometriosis is an estrogen-dependent disease characterized by ectopic growth of endometrium-like glands and stroma outside the uterus. It has a considerable impact on endometrial receptivity: it is estimated, that 6%-10% of women in general and 35%-50% of women with pelvic pain or infertility suffer from the disease. Noteably, the expression of numerous microRNAs is dysregulated in endometriosis. microRNAs are small non-coding RNAs which regulate gene expression at the posttranscriptional level. Here, we characterize the functional impact of one microRNA previously show to be dysragulated in endometriosis – miR-218 – using an in vitro system. Emplyoing the human endometriotic epithelial cell line 12Z, we are able to demonstrate that miR-218 upregulation via transient transfection of precursor molecules results in reduced invasiveness in matrigel invasion chamber and in reduced cell viability. qPCR analysis in 12Z cells, in the endometrial stroma cell line St-T1b, and in patient-derived primary endometrial stroma cells reveled a significant downregulation of two predicted targets of miR-218, the epidermal growth factor receptor EGFR, and the proteoglycan decorin. While EGFR expression has been shown to be upregulated in severe versus mild disease, decorin is known to be expressed in an estrogen-dependent manner in the endometrium. Current investiations are therefore focussing on a detailed analysis of the contribution of these factors to the miR-218-dependent phenotype, since decorin contributes to the pathogenesis of malignant and inflammatory diseases by influencing angiogenesis and matrix-dependent signalling via TGFbeta and by interferon gamma signalling during inflammation. Furthermore, EGFR is involved in the regulation of cell proliferation, invasiveness and epithelial-to-mesenchymal transition, rendering these two factors promising candidates for the miR-218-dependent pathogenetic mechanism.
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