ArticleJournal of translational medicine2026
HMGN2 deficiency drives DLBCL progression through impaired R-loop formation and PI3K-AKT hyperactivation.
Article in Journal of translational medicine, 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
backgroundDiffuse large B-cell lymphoma (DLBCL) exhibits significant heterogeneity, with therapy resistance in Activated B-cell-like (ABC) and relapsed Germinal Center B-cell-like (GCB) subtypes being major challenges, with underlying drivers poorly understood.
methodsWe performed single-cell RNA sequencing (scRNA-seq) on de novo ABC-DLBCL, de novo GCB-DLBCL, and relapsed GCB-DLBCL specimens. Analyses included malignant cell subclustering, R-loop scoring, trajectory inference, and cell-cell communication. HMGN2 was functionally validated in vitro.
resultsWe identified an aggressive, poor-prognosis B-cell subpopulation in de novo ABC and relapsed GCB-DLBCL, defined by significantly reduced R-loop formation.This phenotype was directly associated with the downregulation of High-Mobility Group Nucleosome Binding Domain 2 (HMGN2). Mechanistically, we validated that HMGN2 promotes R-loop formation; its loss derepresses IL4R expression, leading to hyperactivation of the oncogenic PI3K-AKT signaling pathway. Functional validation confirmed that HMGN2 knockdown in DLBCL cell lines enhanced proliferation and clonogenicity, whereas its overexpression was inhibitory. The tumor microenvironment in relapsed GCB tumors exhibited profoundly immunosuppressive features, including functionally impaired CD8+T cells and dominant inhibitory BTLA-TNFRSF14 interactions.
conclusionsOur study identifies a potential HMGN2/R-loop/PI3K-AKT axis that may drive malignant cell-intrinsic fitness while shaping an immune-suppressive microenvironment. These findings position HMGN2 as a candidate regulator of DLBCL progression and a potential prognostic biomarker and therapeutic target to address treatment resistance.
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