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A comprehensive analysis of the mechanism of FOS in the progression of endometrialcyst of ovary to endometriosis-associated ovarian cancer

ABSTRACT: Background: Endometrialcyst of ovary (EMC) may develop into endometriosis-associated ovarian cancer over time (EAOC). EAOC pathogenesis is unknown. This study investigated the likely mechanism of EAOC publishing related with orthotopic endometrial, searched for a feasible biomarker using RNA sequencing, and examined the molecular function of this biomarker in ectopic endometrial cells from EAOC and EMC patients. Methods: RNA sequencing was performed on 5 EAOC and 4 EMC tissue samples. Differential expression analysis employed RNA-seq data. To identify biomarkers, differential genes were used in PPI network design, GO pathway enrichment, and GSEA pathway enrichment. Immunohistochemical staining revealed FOS expression in various endometrium. Lv-FOS was utilized to up-regulate FOS in hEnSCs, and cell counting kit-8 (CCK-8), colony formation assay, and scratch assay were performed to assess cell viability, proliferation, and migration. Western blot showed protein expression alterations. Results: 249 genes were differently expressed, including FOS. Pathway enrichment study demonstrated that MAPK, AP-1, ERK, and other signaling pathways were involved in EMC-to-EAOC conversion. FOS upregulation in hEnSCs increased cell viability, proliferation, and migration. Western blot results showed that FOS, CDK4, cyclinD1, P21, and invasion-related proteins p-stat3, MMP2, and MMP9 were up- or down-regulated, respectively. Conclusion: Mitosis and cell cycle affect EMC to EAOC progression. FOS expression, a novel biomarker, promotes EMC transition into EAOC and endometrial cell proliferation, invasion, and migration. Keywords: FOS, endometrialcyst of ovary, endometriosis-associated ovarian cancer, biomarker

ORGANISM(S): Homo sapiens

PROVIDER: GSE226575 | GEO | 2023/05/23

REPOSITORIES: GEO

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Project description:Endometriosis is a debilitating gynecological disorder affecting approximately 10% of the female population. Despite its prevalence, robust methods to classify and treat endometriosis remain elusive. Changes throughout the menstrual cycle in tissue size, architecture, cellular composition, and individual cell phenotypes make it extraordinarily challenging to identify markers or cell types associated with uterine pathologies since disease-state alterations in gene and protein expression are convoluted with cycle phase variations. Here, we developed an integrated workflow to generate both proteomic and single-cell RNA-sequencing (scRNA-seq) data sets using tissues and cells isolated from the uteri of control and endometriotic donors. Using a linear mixed effect model (LMM), we identified proteins associated with cycle stage and disease, revealing a set of genes that drive separation across these two biological variables. Further, we analyzed our scRNA-seq data to identify cell types expressing cycle and disease- associated genes identified in our proteomic data. A module scoring approach was used to identify cell types driving the enrichment of certain biological pathways, revealing several pathways of interest across different cell subpopulations. Finally, we identified ligand-receptor pairs including Axl/Tyro3 – Gas6, that may modulate interactions between endometrial macrophages and/or endometrial stromal/epithelial cells. Analysis of these signaling pathways in an independent cohort of endometrial biopsies revealed a significant decrease in Tyro3 expression in patients with endometriosis compared to controls, both transcriptionally and through histological staining. This measured decrease in Tryo3 in patients with disease could serve as a novel diagnostic biomarker or treatment avenue for patients with endometriosis. Taken together, this integrated approach provides a framework for integrating LMMs, proteomic and RNA-seq data to deconvolve the complexities of complex uterine diseases and identify novel genes and pathways underlying endometriosis.

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A comprehensive analysis of the mechanism of FOS in the progression of endometrialcyst of ovary to endometriosis-associated ovarian cancer

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