ArticleFrontiers in cell and developmental biology2026
Integrated multi-omics characterization of SPTBN2 overexpression reveals its pro-tumorigenic role and immune microenvironment remodeling in colorectal cancer.
Article in Frontiers in cell and developmental biology, 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
Background: Colorectal cancer (CRC) is highly heterogeneous, which limits the consistency of benefit from immune checkpoint blockade. SPTBN2 has recently been implicated as a candidate biomarker in CRC, but its cross-omics features and potential links to the tumor immune microenvironment remain insufficiently characterized. Methods: We integrated multi-omics profiles from TCGA and GEO, including transcriptomics and DNA methylation, to evaluate SPTBN2 expression patterns, prognostic relevance, and epigenetic associations. Single-cell RNA sequencing (scRNA-seq) and spatial transcriptomics were used to localize SPTBN2 across cellular compartments and to contextualize immune states. Mendelian randomization (MR) and summary-data-based MR (SMR) analyses were applied to prioritize candidate genes genetically associated with CRC risk. Results: SPTBN2 was consistently upregulated in CRC tissues and was associated with poorer overall survival, remaining significant after adjustment for clinical covariates. Promoter-region hypomethylation showed an inverse association with SPTBN2 mRNA abundance, a pattern consistent with epigenetic derepression. Immune profiling further indicated that higher SPTBN2 expression co-occurred with an immune-inhibitory milieu, including increased regulatory T-cell signatures and elevated expression of inhibitory checkpoints (e.g., PD-1 and CTLA-4), suggestive of an immunogenic-yet-suppressed state. Integrating MR/SMR prioritization with scRNA-seq highlighted S100P and VSIG2 as downstream candidates; functional assays supported their roles in tumor cell proliferation. Conclusion: Collectively, these multi-layer data position SPTBN2 as a research-stage prognostic biomarker in CRC and support a mechanistic hypothesis linking SPTBN2-high tumors to immune inhibitory programs. Direct perturbation of SPTBN2 and independent clinical validation are warranted to establish functional causality and translational utility.
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