ArticleScientific reports2025
Single-cell and bulk transcriptomics uncovers PRKD2-driven tumor stemness and progression in multiple myeloma.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Corrections and comments
- Erratum issued
Authors and funding
14 authors.
Funding
Abstract
Multiple myeloma (MM) remains incurable, as most patients relapse or become refractory (RRMM), and the molecular nexus among clonal evolution, immune escape and therapy response remains unknown. Bulk RNA-seq from 24 MM to 6 matched marrows (subset of 132) plus single-cell datasets were analysed by differential expression, pseudotime, WGCNA, enrichment, immune deconvolution and GDSC drug screens. PRKD2 was knocked down (KD) or over-expressed (OE) in H929, 8226 and U266 cells. Viability (CCK-8) and apoptosis (Annexin V/7-AAD) were assessed after 48 h of axitinib (1.25-10 µM). PRKD2 was the sole gene uniformly up-regulated in newly diagnosed MM, RRMM and poor-survival cohorts, rising along the malignant plasma-cell trajectory. High PRKD2 aligned with ISS-III stage, elevated mRNAsi/EREG_mRNAsi and worse 5-year survival (38% vs. 73%, P = 0.012). PRKD2-KD reduced proliferation (~ 30%) and restored HLA-E, whereas PRKD2-OE suppressed antigen-presentation genes and polarised macrophages toward an IL-6/MERTK tumour-promoting phenotype. PRKD2-high marrow contained more naïve/memory B cells but fewer mature plasma cells. PRKD2 expression correlated positively with axitinib sensitivity (- log
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