Upregulation of fibroblast growth factor 2 contributes to endometriosis through SPRYs/DUSP6/ERK signaling pathway

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Fibroblast growth factor 2 (FGF2) upregulation promotes endometriosis by activating the SPRY/DUSP6/ERK signaling pathway.

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Abstract

Previous studies report that fibroblast growth factor 2 (FGF2) modulates Sproutys (SPRYs)/dual specificity phosphatase 6 (DUSP6)/extracellular signal-regulated kinase (ERK) signaling pathway in endometrial glandular epithelial cells. However, its role in endometriosis remains unclear. The expression patterns and localization of related proteins in endometrium patients' samples were determined using quantitative reverse transcription PCR, Western blotting, and immunohistochemistry, respectively. Human endometrial stromal cells (HESCs) were isolated and transfected with small interfering RNA (siRNA) targeting FGF2 (FGF2-siRNA). Cell viability was determined using 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. It was found that FGF2 mRNA and protein levels were increased in the ectopic endometrium, whilst the mRNA and protein levels of SPRYs/DUSP6/ERK signaling pathway related-genes were dysregulated. Spearman's rank correlation analysis revealed a negative correlation between FGF2 and SPRYs/DUSP6 signaling pathway-related proteins. In vitro study demonstrated that FGF2 silencing suppressed cell proliferation. Our results suggest that FGF2 upregulation might contribute to endometriosis via the regulation of the SPRYs/DUSP6/ERK signaling pathway.

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Condition tags

endometriosis

MeSH descriptors

Dual Specificity Phosphatase 6 Endometriosis Extracellular Signal-Regulated MAP Kinases Fibroblast Growth Factor 2 Membrane Proteins Phosphoproteins Cell Line, Tumor Cell Proliferation Cell Survival Dual Specificity Phosphatase 6 Endometriosis Endometrium Endometrium Epithelial Cells Epithelial Cells Extracellular Signal-Regulated MAP Kinases Female Fibroblast Growth Factor 2 Gene Silencing Humans

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europepmc
last seen: 2026-07-28T06:14:09.330459+00:00
openalex
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