ArticleHereditas2026
Extracellular matrix-growth factor signalling drives the oncogenic mir-125b-2/UCK2 axis in hepatocellular carcinoma.
Article in Hereditas, 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Authors and funding
8 authors.
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Abstract
backgroundHepatocellular carcinoma (HCC) is characterized by coordinated transcriptional and post-transcriptional dysregulation. We sought to identify clinically relevant miRNA–mRNA regulatory axes with cross-cohort, multi-layer validation.
methodsTumor–normal differential expression was integrated across TCGA-LIHC and independent microarray cohorts. Predicted miRNA targets were filtered by inverse-direction overlap with consensus DEGs and evaluated for activity–abundance coherence and survival relevance. An eight-feature axis (four miRNAs and four target-set activities) was modeled using penalized Cox regression with cross-validation and externally validated.
resultsFour recurrent miRNAs were identified (miR-125b-2 downregulated; miR-21, miR-221, miR-9-1 upregulated). miR-125b-2 showed the strongest inverse coherence with its target set (ρ = −0.41, P < 1 × 10⁻¹²). The composite axis stratified TCGA overall survival (log-rank P < 0.0001) and validated in GSE31384 (HR = 1.62, 95% CI 1.15–2.28; C-index = 0.66). Seven targets met FDR ≤ 1%, with UCK2 exhibiting the strongest adverse association (HR = 2.78, P = 2.7 × 10⁻⁹). UCK2 was overexpressed, hypomethylated, enriched in epithelial compartments, and linked to proliferative and ECM/growth-factor signaling programs. Functional assays demonstrated that UCK2 knockdown suppressed proliferation, clonogenicity, and migration, whereas overexpression enhanced these phenotypes.
conclusionsThe miR-125b-2/UCK2 axis defines a metabolically driven, epithelial proliferative program coupled to ECM/GF signaling and represents a validated prognostic and biologically actionable node in HCC.
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