ArticleScientific reports2020
Bioinformatic analysis reveals the importance of epithelial-mesenchymal transition in the development of endometriosis.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 85 citations in OpenAlex.
- Natural Products Targeting Oxidative Stress-Inflammation Crosstalk in Endometriosis.American journal of reproductive immunology (New York, N.Y. : 1989) · 2026Review
- Peritoneal Incretin Deficiency and Tirzepatide as a Multi-Axis Adjuvant Hypothesis in Treatment-Refractory Endometriosis: A Mechanistic Framework Linking Metabolism, Immunity, Fibrosis, and Nociception.International journal of molecular sciences · 2026Review
- ML-Driven Pharmaceutical Cocrystal Technology: Advances in Screening, Property Prediction and Applications.AAPS PharmSciTech · 2026Review
- Inhibition of CDC42 in adenomyosis reduces the proliferation of endometrial stromal cells and the migration of epithelial cells.American journal of translational research · 2026Article
- Bioinformatic analysis and validation of candidate genes in the eutopic endometrium reveal differential expressions in diffuse adenomyosis, endometrioma, and their co-existence.European journal of medical research · 2025Article
- Identification of shared pathogenetic mechanisms between endometriosis and RSA based on comprehensive bioinformatics analysis.Journal of assisted reproduction and genetics · 2025Article
- D-chiro-inositol effectively counteracts endometriosis in a mouse model.Molecular medicine (Cambridge, Mass.) · 2025Article
- Potential Modulatory Role of Phoenixin-14 in Epithelial-Mesenchymal Transition of Endometriotic 12Z Cells.Biomedicines · 2025Article
- Identification and Characterization of m6A Regulators METTL3 and YTHDF2: Unveiling Their Biological Functions in Endometriosis.International journal of women's health · 2025Article
- Upregulation of miR-183 inhibits the invasion and migration of endometrial stromal cells in endometriosis patients by downregulating Ezrin.Frontiers in oncology · 2025Article
- CADM2 participates in endometriosis development by influencing the epithelial-mesenchymal transition.Reproductive sciences (Thousand Oaks, Calif.) · 2024Article
- PDLIM3 knockdown promotes ferroptosis in endometriosis progression via inducing Gli1 degradation and blocking Hedgehog signaling pathway.Journal of assisted reproduction and genetics · 2024Article
- Unraveling pathogenesis, biomarkers and potential therapeutic agents for endometriosis associated with disulfidptosis based on bioinformatics analysis, machine learning and experiment validation.Journal of biological engineering · 2024Article
- The Different Gene Expression Profile in the Eutopic and Ectopic Endometrium Sheds New Light on the Endometrial Seed in Endometriosis.Biomedicines · 2024Review
- MLLT11 Regulates Endometrial Stroma Cell Adhesion, Proliferation and Survival in Ectopic Lesions of Women with Advanced Endometriosis.International journal of molecular sciences · 2023Article
- Signatures of necroptosis-related genes as diagnostic markers of endometriosis and their correlation with immune infiltration.BMC women's health · 2023Article
- Exosomes: potential diagnostic markers and drug carriers for adenomyosis.Frontiers in pharmacology · 2023Review
- Integrated bioinformatic analysis of dysregulated microRNA-mRNA co-expression network in ovarian endometriosis.Acta obstetricia et gynecologica Scandinavica · 2022Article
- What Do the Transcriptome and Proteome of Menstrual Blood-Derived Mesenchymal Stem Cells Tell Us about Endometriosis?International journal of molecular sciences · 2022Article
- SIRT1 upregulation promotes epithelial-mesenchymal transition by inducing senescence escape in endometriosis.Scientific reports · 2022Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundEndometriosis is a frequently occurring disease in women, which seriously affects their quality of life. However, its etiology and pathogenesis are still unclear.
methodsTo identify key genes/pathways involved in the pathogenesis of endometriosis, we recruited 3 raw microarray datasets (GSE11691, GSE7305, and GSE12768) from Gene Expression Omnibus database (GEO), which contain endometriosis tissues and normal endometrial tissues. We then performed in-depth bioinformatic analysis to determine differentially expressed genes (DEGs), followed by gene ontology (GO), Hallmark pathway enrichment and protein-protein interaction (PPI) network analysis. The findings were further validated by immunohistochemistry (IHC) staining in endometrial tissues from endometriosis or control patients.
resultsWe identified 186 DEGs, of which 118 were up-regulated and 68 were down-regulated. The most enriched DEGs in GO functional analysis were mainly associated with cell adhesion, inflammatory response, and extracellular exosome. We found that epithelial-mesenchymal transition (EMT) ranked first in the Hallmark pathway enrichment. EMT may potentially be induced by inflammatory cytokines such as CXCL12. IHC confirmed the down-regulation of E-cadherin (CDH1) and up-regulation of CXCL12 in endometriosis tissues.
conclusionsUtilizing bioinformatics and patient samples, we provide evidence of EMT in endometriosis. Elucidating the role of EMT will improve the understanding of the molecular mechanisms involved in the development of endometriosis.
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