ArticleDiscover oncology2026
Cell type-resolved analysis identifies LOXL2⁺ fibroblasts as key drivers of malignant stromal remodeling in hepatocellular carcinoma.
Article in Discover oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Hepatocellular carcinoma (HCC) typically progresses within a fibrotic, collagen-rich microenvironment where extracellular matrix (ECM) remodeling critically dictates tumor malignancy. However, the cell-type-specific contributions of the lysyl oxidase (LOX) family to this remodeling remain poorly understood. In this study, we conducted an integrative transcriptomic analysis of the LOX gene family (LOX, LOXL1-4) in HCC. Bulk RNA-seq analysis revealed that LOX, LOXL2, and LOXL4 were significantly upregulated in tumors and correlated with advanced pathological stages and poor prognosis. Single-cell RNA-seq (scRNA-seq) analysis delineated distinct expression landscapes: LOX and LOXL4 were enriched in malignant cells, while LOXL2 was predominantly expressed in fibroblasts and endothelial cells. Notably, we identified a discrete LOXL2⁺ fibroblast subset characterized by transcriptomic programs associated with ECM remodeling, contractility, angiogenesis, and hypoxia. A signature derived from LOXL2⁺ fibroblasts was significantly associated with inferior overall survival and enhanced epithelial-mesenchymal transition (EMT) activity in the TCGA-LIHC cohort. Intercellular signaling analysis (CellChat) demonstrated that LOXL2⁺ fibroblasts engage in robust crosstalk with malignant cells via collagen/periostin-integrin signaling axes. Finally, STIP1 was identified through LASSO and random survival forest models as a critical prognostic effector within the LOXL2⁺ fibroblast program. Our findings establish LOXL2⁺ fibroblasts as a pivotal stromal subset driving malignant remodeling and provide potential therapeutic targets for HCC.
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