ArticleFEBS open bio2020
ADAMTS7 degrades Comp to fuel BMP2-dependent osteogenic differentiation and ameliorate oncogenic potential in osteosarcomas.
Article in FEBS open bio, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 11 citations in OpenAlex.
- TNF-α orchestrates ADAM metallopeptidase with thrombospondin type 1 motif 2 upregulation and extracellular matrix remodeling through multimodal signaling in osteosarcoma cells.Molecular biology reports · 2026Article
- Single-cell profiling of bone metastasis ecosystems from multiple cancer types reveals convergent and divergent mechanisms of bone colonization.Cell genomics · 2025Article
- Construction of store-operated calcium entry-related gene signature for predicting prognosis and indicates immune microenvironment infiltration in stomach adenocarcinomas.Scientific reports · 2024Article
- Application of second-generation sequencing in congenital pulmonary airway malformations.Scientific reports · 2022Article
- Cartilage Oligomeric Matrix Protein, Diseases, and Therapeutic Opportunities.International journal of molecular sciences · 2022Review
- Strategies for Improving Photodynamic Therapy Through Pharmacological Modulation of the Immediate Early Stress Response.Methods in molecular biology (Clifton, N.J.) · 2022Review
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7 authors at 1 institution in 1 country.
Funding
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Abstract
Osteosarcoma (OS) is the most common primary malignant bone tumor in children and adolescents, with a high metastatic potential. Despite dramatic changes in OS treatments over the past decades, their efficiency still remains limited, with severe complications and adverse side effects. Key mechanisms underlining tumorigenesis, metastasis and chemotherapy resistance are currently lacking, in turn hindering any progress with respect to developing effective and safe therapeutic strategies against OS. Recently, ADAMTS7, a member of the disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS) family, was shown to be involved in osteogenic differentiation-related pathological processes. ADAMTS7 promotes vascular calcification via disturbing the balance between osteogenic bone morphogenetic protein (BMP)2 (regulating osteogenic differentiation and bone formation during development) and its natural inhibitor cartilage oligomeric matrix protein (Comp). Hence, in the present study, we aimed to investigate the role of ADAMTS7 in the pathological process of OS. We first revealed that ADAMTS7 was decreased in OS tissues. Lower expression of ADAMTS7 was correlated with poor histological differentiation and an advanced clinical stage of OS. Through loss- and gain-function analysis, we further revealed that ADAMTS7 attenuated cell proliferation, migration and invasion, at the same time as promoting the expression of osteogenic differentiation markers in two OS cell lines: MG63 and SAOS2. Moreover, Comp was responsible for the effects of ADAMTS7 on OS pathogenesis by reinforcing cell osteogenic differentiation mediated by BMP2 in vitro. In conclusion, ADAMTS7-mediated degradation of Comp may provide a potential therapeutic target for the treatment of OS.
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