ArticleStem cell research & therapy2025
Unveiling the role of gastric cancer-associated mesenchymal stem cells and neutrophil extracellular traps through multi-omics analysis.
Article in Stem cell research & therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Roles of neutrophil extracellular traps in cancer immunotherapy resistance and therapeutic targeting.Biomarker research · 2026Review
- Rearming mesenchymal stem cells with engineering strategies to combat cancer.Frontiers in immunology · 2026Review
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGastric cancer (GC) is a highly aggressive malignancy with a poor prognosis, closely linked to the tumor microenvironment (TME). Emerging evidence highlights the critical role of gastric cancer-associated mesenchymal stem cells (GC-MSCs) in recruiting neutrophils and facilitating neutrophil extracellular traps (NETs) formation, thereby remodeling the tumor microenvironment (TME) and promoting tumor progression, immune modulation, and metastasis.
methodsThis study integrated single-cell RNA sequencing (scRNA-seq), Mendelian randomization (MR), and functional enrichment analyses to uncover the molecular underpinnings of GC. Transcriptomic data from public databases, including TCGA and GEO, were analyzed to explore cellular heterogeneity and the influence of NETs within the TME. MR analysis was conducted to establish causal relationships between key NET-related genes and GC. We integrated scRNA-seq, MR, and functional enrichment analyses to systematically dissect the roles of GC-MSCs and NETs in reshaping the tumor microenvironment.
resultsscRNA-seq identified 12 distinct cell types in the TME, with significantly elevated NET scores associated with GC-MSCs in the disease group. Functional enrichment analyses revealed that NET-associated marker genes were enriched in pathways such as oxidative phosphorylation and cytoplasmic translation. MR analysis confirmed EIF1 and RPS12 as key genes with causal links to GC progression, demonstrating robust associations with immune cell infiltration and critical signaling pathways. Additionally, transcriptional regulation analysis identified motifs and transcription factors governing these genes, while GSEA highlighted their involvement in pathways such as ribosome biogenesis and focal adhesion.
conclusionThis study elucidates the intricate interplay between GC-MSCs, NETs, and the immune microenvironment, offering novel insights into GC pathogenesis and potential therapeutic targets. EIF1 and RPS12 emerge as promising candidates for precision medicine, with broader implications for NET-related cancer research.
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