ArticleFrontiers in immunology2025
Neutrophil elastase promotes low molecular weight cyclin E1 formation to accelerate osteosarcoma proliferation.
Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- From Bone Marrow Reserve to Metastatic Niche: How Neutrophil-Lineage Cells Shape Skeletal Colonization.International journal of molecular sciences · 2026Review
- Review
- Metabolic-immune crosstalk in osteosarcoma: mechanisms and therapeutic opportunities.Frontiers in immunology · 2026Review
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Authors and funding
6 authors.
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Abstract
Introduction: Osteosarcoma (OS) is the most common primary bone malignancy, characterized by aggressive local invasion and a high propensity for metastasis. We previously reported that cyclin E1 is upregulated in osteosarcoma. In this study, we identified a cytoplasmic, low molecular weight cyclin E1 isoform (LMW-cyclin E1) in osteosarcoma that is significantly associated with poor patient outcomes. Methods: We collected RNA sequencing data to analyze the cyclin E1 ( Results and discussion: Mechanistically, we found that ELA2, primarily derived from tumor-associated neutrophils, cleaves full-length cyclin E1 to generate LMW-cyclin E1, which accelerates OS proliferation. Moreover, neutrophil infiltration was associated with OS lung metastasis. OS cells also induced neutrophil extracellular trap formation, which further amplified ELA2 release. Depleting neutrophils or inhibiting ELA2 significantly suppressed OS malignancy. Hence, targeting neutrophil-osteosarcoma crosstalk may be a potential novel therapeutic strategy.
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