ArticleFrontiers in cell and developmental biology2025
Single-cell sequencing reveals cell heterogeneity and aberrantly activated pathways associated with microvascular invasion in hepatocellular carcinoma.
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 3 papers.
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3 citing papers in PubMed.
- Structural architecture of collagen and collagen-fibronectin networks is associated with the invasive behavior of liver cancer cells.Cellular oncology (Dordrecht, Netherlands) · 2026Article
- Exploring single-cell and multi-omics technologies and their role in unraveling tumor heterogeneity of hepatocellular carcinoma.Journal of liver cancer · 2026Review
- Mechanisms and therapeutic strategies of bidirectional crosstalk between hepatic stellate cell-derived cancer-associated fibroblasts and T cells in immune evasion and therapeutic resistance of hepatocellular carcinoma.Frontiers in immunology · 2026Review
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4 authors.
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Abstract
Introduction: Hepatocellular carcinoma (HCC) is the most common primary liver cancer, with microvascular invasion (MVI) identified as a major predictor of early recurrence. However, the intratumor cellular heterogeneity of MVI, the identification of pertinent biomarkers, and the role of intercellular signalling interactions in MVI progression are unclear. This study aims to explore these aspects using single-cell transcriptomic analysis. Methods: The present study utilized single-cell transcriptomic data from public databases to conduct an in-depth transcriptome analysis of tumour tissues and adjacent nontumor tissues from five patients with hepatocellular carcinoma, with a particular focus on samples from three patients exhibiting microvascular invasion. Bioinformatics tools were employed to analyze gene expression patterns and signalling pathways. Results: The findings indicated that MVI-positive malignant cells activate multiple signalling pathways to facilitate invasion and metastasis. Specific malignant cell subtypes strongly associated with MVI were identified, exhibiting distinctive gene expression patterns related to proliferation, invasion, and metabolic reprogramming of tumour cells. Further analysis revealed that the laminin and VEGF signalling pathways are crucial for remodelling the tumour microenvironment and angiogenesis associated with MVI. The MARCKSL1 gene was predominantly expressed in MVI-positive malignant cells and may contribute to MVI progression by interacting with the PTN signalling network. Additionally, MARCKSL1 is linked to tumour resistance to multiple anticancer drugs. Discussion: This study sheds light on the molecular characteristics and functional heterogeneity of MVI-associated malignant cell subpopulations. The single-cell transcriptome and bioinformatics analyses provided insights into the mechanisms driving MVI, potentially aiding the development of targeted diagnostic and therapeutic strategies. Future research should further validate the role of MARCKSL1 in MVI progression and explore its potential clinical applications.
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