ArticleMolecular and cellular biochemistry2026
ELANE inhibits the progression of osteosarcoma via suppressing the CXCL12/CXCR4 axis.
Article in Molecular and cellular biochemistry, 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
We aimed to screen novel biomarkers for osteosarcoma (OS) using bioinformatics analysis and explore their regulatory mechanisms in OS progression. Differentially expressed genes (DEGs) were screened from GSE36001 and GSE19276 datasets. Hub genes were isolated from protein-protein interaction networks and subsequently validated using real-time quantitative polymerase chain reaction, with their expression patterns further confirmed in an independent external cohort (GSE16088 dataset). The role of neutrophil elastase (ELANE) in OS was assessed using immunohistochemical staining of Ki67 and hematoxylin-eosin staining in a subcutaneous tumor experiment. The proliferation, migration, invasion, and apoptosis were determined using Cell Counting Kit-8, wound healing, Transwell, and flow cytometry assays. A total of 71 overlapping DEGs related to OS were identified. ELANE, AZU1, DEFA4, RNASE3, PRTN3, and CTSG were identified as hub genes of OS, which were down-regulated in OS cells. ELANE was selected as the research target. Overexpression of ELANE inhibited tumor growth in OS. In vitro experiment, overexpression of ELANE suppressed the proliferation, migration, and invasion, while promoting apoptosis of OS cells. Conversely, its silencing had the opposite effect. Furthermore, chemokine signaling pathway was selected as the downstream pathway of ELANE in OS. ELANE inhibited the expression of CXCL12 and CXCR4. The activation of CXCL12/CXCR4 axis reversed the inhibitory impact of ELANE on the proliferation, migration, and invasion, as well as the promoting effects of ELANE on apoptosis of OS cells. ELANE was a novel gene signature of OC, which exerts an anti-tumor effect on OS progression via inhibiting CXCL12/CXCR4 axis.
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