ArticleAmerican journal of translational research2025
MEGF8-driven metabolic reprogramming and immune evasion define a high-risk subtype of endometriosis-associated ovarian cancer.
Article in American journal of translational research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Novel Exploratory Transcriptomic Candidates as Biomarkers and Cancer Hallmark Fingerprints for Ovarian Endometroid and Clear Cell Carcinomas in Women.Antioxidants (Basel, Switzerland) · 2026Article
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13 authors.
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Abstract
objectiveEndometriosis increases ovarian cancer (OC) risk through genetic mutations, chronic inflammation, and hormonal dysregulation, yet the underlying molecular pathways remain underexplored. This study aims to identify endometriosis-associated prognostic biomarkers in OC.
methodsTranscriptomic and clinical data from TCGA-OC and GSE53963 were integrated for comprehensive analysis. Prognostic models were constructed using LASSO and Cox regression. Tumor microenvironment (TME) characteristics, immune checkpoints, and drug sensitivity were evaluated with ESTIMATE, CIBERSORT, TIDE, and drug sensitivity profiling. Single-cell RNA sequencing (scRNA-seq, GSE184880) was employed to explore immune and gene expression patterns. MEGF8 function was validated through
resultsConsensus clustering identified three OC molecular subtypes (A, B, and C), with subtype B showing significantly better overall survival (P = 0.001). Subtype A exhibited a "dual malignant phenotype", characterized by enhanced cell adhesion, epithelial-mesenchymal transition (EMT), TGF-β activation, and an immunosuppressive TME. An 8-gene prognostic model, including MEGF8, effectively stratified patients into high- and low-risk groups, with high-risk patients showing poorer survival, immune evasion, and elevated stromal scores. Drug sensitivity analysis indicated that the low-risk group was more responsive to PI3K/AKT/mTOR and VEGFR inhibitors. MEGF8 was identified as a key regulator in cancer stem cells, promoting tumor progression through metabolic reprogramming and extracellular matrix remodeling. Functionally, MEGF8 knockdown suppressed OC cell proliferation and migration.
conclusionThis study delineated the molecular-immune landscape of OC, established an 8-gene prognostic model, and identified MEGF8 as a potential therapeutic target. The model predicts responses to immunotherapy and targeted therapies, supporting personalized OC management.
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