ArticleFrontiers in cell and developmental biology2025
A spatially resolved single-cell landscape of colorectal cancer liver metastasis reveals a stromal-tumor glycolytic signaling interaction.
Article in Frontiers in cell and developmental biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed.
- Integrated single-cell and spatial transcriptomic analyses reveal malignant epithelial glycolytic heterogeneity and spatial niche remodeling during colorectal cancer progression.Functional & integrative genomics · 2026Article
- Neutrophil extracellular traps in colorectal cancer: context-dependent roles from inflammatory carcinogenesis to liver metastasis and therapeutic targeting.Journal of translational medicine · 2026Review
- Multi Omics Integration in Colorectal Cancer: From Molecular Insights to Precision Oncology.Cancers · 2026Review
- Metastatic Odyssey: Decoding the Genomic Journey from Primary Colorectal Cancer to Disseminated Disease.Cancers · 2026Review
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Abstract
Background: Colorectal cancer (CRC) remains a leading cause of cancer mortality, with liver metastasis being the principal determinant of poor prognosis, but the spatial mechanisms orchestrating metastatic niches remain elusive. Method: To dissect the molecular and spatial dynamics of CRC progression, we constructed an integrative atlas using 35 single-cell RNA-seq datasets and spatial transcriptomics from primary tumors, liver metastases, and matched normal tissues. Malignant epithelial subpopulations were stratified via inferCNV and CytoTRACE analyses. Stromal-tumor interactions were dissected using CellChat and NicheNet, with functional validation through Result: We identified a transcriptionally distinct epithelial subpopulation, termed high-malignancy CRC (High-M CRC), enriched in metastatic lesions and characterized by enhanced stemness, MYC-driven transcriptional activity, and glycolytic reprogramming. Stromal-tumor interaction analyses revealed that cancer-associated fibroblasts (CAFs), particularly matrix CAFs (mCAFs), promote malignant progression via the HGF-MET-MYC signaling axis. Spatial transcriptomic mapping confirmed the physical proximity and molecular co-localization of High-M CRC cells and mCAFs, along with enriched glycolysis and MYC expression at the cell-cell interface. Conclusion: We unveil a spatially organized metabolic niche driven by stromal-tumor HGF-MET-MYC signaling. These findings offer novel insights into the stromal-tumor interaction and suggest actionable targets for therapeutic intervention in CRC.
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