ArticleApplied biochemistry and biotechnology2026
Identification and Validation of the Breast Cancer Diagnostic Biomarker SVEP1 and Its Relationship With CD8 + T Cell Activation Using Bioinformatics and Machine Learning.
Article in Applied biochemistry and biotechnology, 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
Breast cancer (BC) is a malignant disease with high mortality. Sushi, von Willebrand factor type A, EGF and pentraxin domain containing 1 (SVEP1) has been reported to exert tumor-suppressive effects in various cancers when overexpressed; nevertheless, its role in BC development remains unknown. The Cancer Genome Atlas (TCGA) and ImmPort were mined for BC differentially expressed genes; machine learning plus single gene set enrichment analysis (GSEA) nominated SVEP1 and its pathways. Tumor Immune Estimation Resource (TIMER) and receiver operating characteristic (ROC) analyses tested SVEP1 as a biomarker and its association with CD8+ T cell infiltration. qPCR and Western blot quantified cellular SVEP1; Western blot, ELISA and EdU assays measured CD8+ T cell granzyme B (GzmB) and Cluster of Differentiation 69 (CD69) levels, IFN-γ/TNF-α/IL-2 secretion and proliferation. CCK8, flow cytometry and Transwell assays tracked BC cell viability, apoptosis, cycle, migration and invasion, and a xenograft model assessed the tumorigenicity of SVEP1-overexpressing cells. A total of 231 differentially expressed genes were identified by analyzing TCGA and ImmPort datasets. Machine-learning algorithms were then applied to intersect the results, yielding three potential candidates: SVEP1, CXC motif chemokine ligand 2 (CXCL2), and enhancer of zeste homolog 2 (EZH2). Single-gene GSEA revealed that SVEP1 was enriched in pathways such as reactome cell cycle checkpoints and reactome membrane traffic. SVEP1 was expressed at low levels in BC. Its overexpression increased the levels of GzmB, CD69, IFN-γ, TNF-α and IL-2 in CD8+ T cells, reduced BC cell viability, promoted apoptosis, and suppressed migration and invasion. Moreover, tumor volume and weight, along with Ki-67 expression, were all significantly decreased in mouse models. These findings demonstrated that SVEP1 is downregulated in BC; restoring its expression promoted CD8+ T cell activation and suppressed BC progression, indicating that SVEP1 perhaps serve as both a diagnostic biomarker and a potential therapeutic target.
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