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by gemini-2.5-flash-lite, 2026-06-07
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This study found that miR-10b targets Syndecan-1, reducing endometriotic cell invasiveness, IL-6 secretion, and MAPK activation, while increasing PAI-1 expression.
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by claude@2026-06, 2026-06-07
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The study investigated how the microRNA miR-10b regulates the heparan sulfate proteoglycan Syndecan-1 (SDC1) and how this affects invasiveness and signaling in endometriotic cells. Using the human endometriotic cell line 12Z and primary eutopic endometrial stromal cells from two ASRM-III patients, the authors used miR-10b precursors or SDC1 siRNA alongside qPCR, Western blotting, luciferase reporter assays, zymography, and invasion/viability assays, with MAPK activation measured by immunoblots. They found that SDC1 knockdown strongly reduced matrigel invasiveness without affecting viability and altered IL-6 secretion and protease activity (reduced MMP-9 expression, reduced MMP-2 activity, increased PAI-1), while miR-10b overexpression downregulated SDC1, reduced invasiveness and cell viability, and decreased HGF-induced MAPK activation; a key limitation is the small patient sample size for primary cells (two patients). This paper is centrally about endometriosis — it tests miR-10b targeting of SDC1 and links it to IL-6 secretion and MAPK signaling controlling endometriotic cell invasiveness.
Abstract
microRNAs are small non-coding RNAs which regulate gene expression at the posttranscriptional and translational level. microRNAs have previously been demonstrated to be dysregulated in endometriosis, a hormone-dependent disease associated with reduced fertility. One of the dysregulated microRNAs is miR-10b, however, its function has not been addressed at the molecular level. Here, we aimed at elucidating the function of the heparan sulfate proteoglycan Syndecan-1 and its potential regulator miR-10b in endometriosis. for this purpose, the human endometriotic cell line 12Z was transiently transfected with Syndecan-1 (SDC1) siRNA or miR-10b precursors and investigated for changes in cell behavior and gene expression. 12Z and primary eutopic endometrial stroma cells of two ASRM-III endometriosis patients were transfected with miR-10b precursors to investigate posttranscriptional regulation of SDC1. qPCR, Western blotting, flow cytometry, 3'UTR luciferase assays and zymography were employed to measure miR-10b-dependent targeting of SDC1, and SDC1-dependent expression changes of proteases and interleukin-6. Altered cell behavior was monitored by matrigel invasion assays, MTT cell viability assays and mitogen activated protein kinase (MAPK) activation blots. Our data showed that SDC1 knockdown inhibited matrigel invasiveness by > 60%, but did not affect cell viability. Interleukin-6 secretion, MMP-9 expression and MMP-2 activity were reduced, while PAI-1 protein expression was upregulated. miR-10b overexpression significantly downregulated SDC1, reduced matrigel invasiveness by 20%, and cell viability by 14%, and decreased MAPK activation in response to hepatocyte growth factor. We conclude that SDC1, a novel target of miR-10b, inhibits epithelial endometriotic cell invasiveness through downregulation of metalloproteinase activity and interleukin-6.
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DOI: 10.1055/s-0033-1336719
Targeting of Syndecan-1 by microRNA miR-10b modulates invasiveness of endometriotic cells via dysregulation of IL-6 secretion and MAPK signaling
microRNAs are small non-coding RNAs which regulate gene expression at the posttranscriptional and translational level. microRNAs have previously been demonstrated to be dysregulated in endometriosis, a hormone-dependent disease associated with reduced fertility. One of the dysregulated microRNAs is miR-10b, however, its function has not been addressed at the molecular level. Here, we aimed at elucidating the function of the heparan sulfate proteoglycan Syndecan-1 and its potential regulator miR-10b in endometriosis. for this purpose, the human endometriotic cell line 12Z was transiently transfected with Syndecan-1 (SDC1) siRNA or miR-10b precursors and investigated for changes in cell behavior and gene expression. 12Z and primary eutopic endometrial stroma cells of two ASRM-III endometriosis patients were transfected with miR-10b precursors to investigate posttranscriptional regulation of SDC1. qPCR, Western blotting, flow cytometry, 3'UTR luciferase assays and zymography were employed to measure miR-10b-dependent targeting of SDC1, and SDC1-dependent expression changes of proteases and interleukin-6. Altered cell behavior was monitored by matrigel invasion assays, MTT cell viability assays and mitogen activated protein kinase (MAPK) activation blots. Our data showed that SDC1 knockdown inhibited matrigel invasiveness by > 60%, but did not affect cell viability. Interleukin-6 secretion, MMP-9 expression and MMP-2 activity were reduced, while PAI-1 protein expression was upregulated. miR-10b overexpression significantly downregulated SDC1, reduced matrigel invasiveness by 20%, and cell viability by 14%, and decreased MAPK activation in response to hepatocyte growth factor. We conclude that SDC1, a novel target of miR-10b, inhibits epithelial endometriotic cell invasiveness through downregulation of metalloproteinase activity and interleukin-6.
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