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Effects of Selenium-mediated RUNX2 Overexpression and its Transcriptome Alterations on Chondrocyte Injury in Kashin Beck disease

GSE311894 Homo sapiens Expression profiling by high throughput sequencing 6 samples Submitted 2025/12/04 Platform GPL24676
Summary
Runt-related transcription factor 2 (RUNX2) is a key regulator of chondrocyte differentiation and apoptosis. To investigate the downstream molecular mechanisms of RUNX2 in chondrocyte injury, we established a RUNX2 overexpression model using lentiviral transfection in human chondrocytes. Total RNA was extracted from RUNX2-overexpressing and control chondrocytes and subjected to RNA sequencing. Differential expression analysis identified 263 upregulated and 216 downregulated genes in RUNX2-overexpressing cells compared with controls. Functional enrichment analysis revealed that these genes were predominantly involved in TNF and MAPK signaling pathways, suggesting that RUNX2 activation promotes inflammatory and apoptotic processes in chondrocytes. These results provide a comprehensive transcriptomic resource for understanding RUNX2-mediated signaling in cartilage degeneration and may contribute to elucidating the molecular pathogenesis of osteoarthropathy such as Kashin-Beck disease.
Published in
Effects of selenium-mediated RUNX2 overexpression and its transcriptome alterations on Chondrocyte injury in Kashin Beck disease
Zhang D, Li Q, Yang X et al. · Frontiers in cell and developmental biology 2025 · PMID 41425094 · doi:10.3389/fcell.2025.1687954
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Also filed as BioProject PRJNA1371909 and SRA study SRP650157. Searching any of these in the dataset finder brings you back here.

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