ArticleJournal of translational medicine2025
SH3BP5-driven metabolic-immune crosstalk in DLBCL: a prognostic biomarker and therapeutic target for reshaping immunosuppressive microenvironment.
Article in Journal of translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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2 citing papers in PubMed.
- Spatiotemporal control of mitoribosome-mediated metabolic reprogramming in cancer: implications for heterogeneity and therapeutic targeting.Frontiers in cell and developmental biology · 2026Review
- Advancements in Nanomedicine for Precision Management of Lymphoma: Mechanisms, Diagnostics, and Therapeutic Strategies.International journal of nanomedicine · 2026Review
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10 authors.
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Abstract
backgroundDiffuse large B-cell lymphoma (DLBCL) is a highly heterogeneous and aggressive hematologic malignancy, with the activated B-cell-like (ABC) subtype displaying particularly poor prognosis due to inherent treatment resistance and elevated recurrence rates. Despite advances in targeted therapies and immunotherapies, a significant proportion of patients experience relapse or refractory disease, highlighting the urgent need for novel biomarkers and innovative therapeutic strategies to improve clinical outcomes.
methodsA multi-dimensional analysis of SH3BP5 expression was performed across DLBCL subtypes, integrating transcriptomic, proteomic, and clinical datasets to assess its correlation with immune infiltration, tumor metabolism, and patient prognosis. Single-cell RNA sequencing data were employed to examine the tumor microenvironment (TME) with higher resolution. Further analysis of the association between SH3BP5 and immune checkpoint gene expression was conducted to explore its potential role in immunotherapy response. Functional in vitro assays were carried out to assess the impact of SH3BP5 knockdown on DLBCL cell proliferation and apoptosis.
resultsThe analysis revealed that SH3BP5 is preferentially overexpressed in the ABC subtype of DLBCL across multiple datasets and validated cohorts, and its high expression is significantly associated with poor overall survival. Single-cell transcriptomic profiling demonstrated that SH3BP5 is mainly expressed in malignant B cells and inversely correlated with immune cell infiltration, particularly CD8 + T cells. Mechanistically, pathway enrichment and metabolic assays indicated that SH3BP5 is linked to mitochondrial metabolic reprogramming, promoting oxidative phosphorylation (OXPHOS) and potentially contributing to reduced responsiveness to immune checkpoint inhibitors (ICIs). Functional studies showed that SH3BP5 knockdown significantly suppressed DLBCL cell proliferation, induced apoptosis, and reduced tumor cell viability in vitro.
conclusionThis study suggests that SH3BP5 may serve as a prognostic biomarker and a potential therapeutic target in DLBCL, particularly within the ABC subtype. By delineating its associations with immune evasion and metabolic reprogramming, these findings provide a mechanistic basis for further exploration of SH3BP5-targeted interventions to help overcome therapy resistance. Future studies in larger clinical cohorts and functional models are warranted to validate these results and assess the potential of integrating SH3BP5 expression profiling into precision medicine strategies for DLBCL.
trial registrationThe study was registered in the Chinese Clinical Trial Registry (ChiCTR2200060430; http://www.chictr.org.cn/ ) on June 1, 2022.
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