ArticleHepatology communications2026
Crosstalk between SPP1+ macrophages and ITGA5+ fibroblasts promotes hepatocellular carcinoma metastasis.
Article in Hepatology communications, 2026. 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.
- IntegratingFrontiers in immunology · 2026Review
- Inflammation in hepatocellular carcinoma progression: a "Single Wick, dual interwoven strands" regulatory framework.Frontiers in immunology · 2026Review
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16 authors.
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Abstract
backgroundHepatocellular carcinoma (HCC) develops from chronic inflammatory conditions to malignancy, with the immune microenvironment playing a significant role in this progression. However, the changes in the dynamic immune microenvironment during the transition from hepatitis to HCC remain poorly understood. Systematic analysis of stage-specific immune microenvironment alterations is essential for identifying therapeutic targets and creating precision strategies for HCC.
methodsUsing single-cell RNA sequencing (scRNA-seq), we created dynamic transcriptome maps of the immune microenvironment across healthy liver, hepatitis, cirrhosis, and HCC stages. Cell-cell communication, trajectory, and enrichment analyses were utilized to characterize relationships between clusters. TCGA-LIHC data were used to validate gene expression and its prognosis. The spatial distribution of ligand-receptor complexes in HCC was confirmed by spatial transcriptomics and multiplexed immunofluorescence. The effects of the tumor microenvironment on cancer cell behavior were examined using co-immunoprecipitation and cell co-culture assays. Finally, the impact of the immune microenvironment on in vivo tumor progression was evaluated using a mouse transplantation model.
resultsWe identified specific immune cell clusters across HCC progression and revealed significant correlations between the abundance of immune cells (macrophages, B cells)and fibroblasts with disease severity. Crosstalk between SPP1+ macrophages and ITGA5+ fibroblasts was observed explicitly in HCC. In vitro and in vivo data demonstrated that the SPP1-ITGA5 interaction triggered the secretion of MMP2 by fibroblasts, thereby promoting malignant progression in HCC.
conclusionsWe present a dynamic transcriptional profile of immune microenvironment evolution during HCC development, aiding in the refinement of diagnostics and the optimization of therapy strategies.
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