microRNA miR-142 - 3 p is a novel regulator of cell viability and proinflammatory signaling in endometrial stroma cells

Christin Susanna Kästingschäfer, Andreas N. Schüring, Ludwig Kiesel, Birgit Gellersen, Martin Götte
In: Experimental and Clinical Endocrinology & Diabetes · 2013 · vol. 121(03) · doi:10.1055/s-0033-1336721 · W2315660815
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Overexpression of miR-142-3p in endometrial stroma cells reduced cell viability and suppressed proinflammatory signaling by downregulating IL6ST and steroid sulfatase, identifying it as a potential therapeutic target for endometriosis.

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This study investigated the functional impact of microRNA miR-142-3p on endometrial stroma cells using both a cell line and primary cells from patients with endometriosis. The researchers found that increased expression of this miRNA significantly reduced cell viability and downregulated the interleukin-6 coreceptor IL6ST, thereby attenuating STAT3 pathway activation and altering NFkB signaling. Additionally, the miRNA suppressed steroid sulfatase expression, indicating a dual role in modulating both cytokine-mediated inflammation and steroid hormone signaling pathways. This paper is centrally about endometriosis — specifically examining molecular mechanisms involving miR-142-3p in endometrial stroma cells relevant to the disease's pathophysiology.

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Abstract

microRNAs (miRNAs) are small, non-coding RNAs which regulate gene expression at the posttranscriptional and translational level. Due to their high regulatory capacity, they are capable of modulating a variety of physiological and pathophysiological processes. Notably, a dysragulation of miRNA expression has been described in hormone-dependent diseases such as endometriosis, a benign condition associated with severe pelvic pain and reduced fertility. In this study, we investigated the functional impact of dysregulated expression of miR-142 – 3 p in the endometrial stroma cell line ST-T1b and in primary endometrial stroma cells from endometriosis patient using a transient transfection approach. Changes in predicted target gene expression were studied by qPCR, whereas changes in cell behaviour were monitored by MTT cell viability assays and Western-blot-based signal transduction analyses. Among different predicted targets, we could demonstrate that increased expression of miR-142 – 3 p resulted in a significantly reduced expression of the interleukin-6-coreceptor IL6ST. miR-142 – 3 p overexpressing cells displayed a reduced IL-6-mediated activation of the STAT3-pathway, and altered basal expression of the transcription fakcor NFkB. Notably, expression of steroid sulfatase, an additional predicted target of miR-143 – 2 p, was significantly downregulated, suggesting an impact of this miRNA both on steroid hormone- and cytokine-mediated signaling events. At the functional level, high expression of this miRNA significantly reduced cell viability. We conclude that miR-142 – 3 p is a novel regulator of cell viability and proinflammatory signaling in endometrial stroma cells, with possible future therapeutic options for endometrial diseases such as endometriosis.
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Subscribe to RSS DOI: 10.1055/s-0033-1336721 microRNA miR-142 – 3 p is a novel regulator of cell viability and proinflammatory signaling in endometrial stroma cells microRNAs (miRNAs) are small, non-coding RNAs which regulate gene expression at the posttranscriptional and translational level. Due to their high regulatory capacity, they are capable of modulating a variety of physiological and pathophysiological processes. Notably, a dysragulation of miRNA expression has been described in hormone-dependent diseases such as endometriosis, a benign condition associated with severe pelvic pain and reduced fertility. In this study, we investigated the functional impact of dysregulated expression of miR-142 – 3 p in the endometrial stroma cell line ST-T1b and in primary endometrial stroma cells from endometriosis patient using a transient transfection approach. Changes in predicted target gene expression were studied by qPCR, whereas changes in cell behaviour were monitored by MTT cell viability assays and Western-blot-based signal transduction analyses. Among different predicted targets, we could demonstrate that increased expression of miR-142 – 3 p resulted in a significantly reduced expression of the interleukin-6-coreceptor IL6ST. miR-142 – 3 p overexpressing cells displayed a reduced IL-6-mediated activation of the STAT3-pathway, and altered basal expression of the transcription fakcor NFkB. Notably, expression of steroid sulfatase, an additional predicted target of miR-143 – 2 p, was significantly downregulated, suggesting an impact of this miRNA both on steroid hormone- and cytokine-mediated signaling events. At the functional level, high expression of this miRNA significantly reduced cell viability. We conclude that miR-142 – 3 p is a novel regulator of cell viability and proinflammatory signaling in endometrial stroma cells, with possible future therapeutic options for endometrial diseases such as endometriosis.

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