ArticleDiscover oncology2026
Multi omics and mechanistic investigation reveals CBFB as a prognostic biomarker in gastric cancer.
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
backgroundGastric cancer is an aggressive malignancy with poor prognosis due to complex pathogenesis, underscoring the need for biomarkers and targets. Core Binding Factor Beta Subunit (CBFB) has regulatory roles across cancers and shows promise, but its prognostic significance and mechanisms in gastric cancer remain unclear.
methodsWe analyzed Gastric cancer transcriptomes by Weighted Gene Co-expression Network Analysis(WGCNA) to identify modules; machine learning prioritized core regulators. Gene Set Enrichment Analysis predicted signaling pathways, and molecular docking validated Core Binding Factor Beta Subunit-Signal Transducer And Activator Of Transcription 3(CBFB-STAT3) interactions. Single-cell RNA-seq was processed with Seurat for Quality control, clustering, and annotation; CellChat quantified intercellular ligand-receptor crosstalk. Functional validation employed Cell Counting Kit-8 proliferation and Transwell migration/invasion assays; Western blot assessed pathway activity.
resultsMulti-omics analyses implicate CBFB in gastric cancer pathogenesis. WGCNA highlighted 40 ribosome biogenesis-related genes, with machine learning prioritizing CBFB as a key regulator. GSEA linked CBFB to the JAK-STAT pathway (NES 1.95). Molecular docking further revealed a high binding affinity between CBFB and STAT3 (ΔG - 11.5 kcal/mol), suggesting a potential interaction. scRNA-seq demonstrated higher CBFB expression in tumor parenchyma, particularly enriched in mast cells. CellChat analysis revealed enhanced mast cell-endothelial crosstalk via COL4A1/COL4A2-CD44 in CBFB-high groups (p < 0.01). Functionally, CBFB knockdown reduced proliferation by ~ 40% and invasion/migration by ~ 30%. Western blot analysis further showed decreased STAT3 phosphorylation and reduced MMP9, suggesting a functional link within a CBFB-STAT3-MMP9 axis crucial for gastric cancer progression.
conclusionCBFB acts as a key player in Gastric cancer progression, with higher expression predicting poor prognosis and showing strong diagnostic potential. Mechanistically, CBFB may promote progression by engaging STAT3; single-cell data indicate overexpression in mast cells with enhanced mast cell-endothelial crosstalk. Functional data support CBFB as a therapeutic target in Gastric cancer.
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