ArticleExperimental and therapeutic medicine2018
Necrosis of osteosarcoma cells induces the production and release of high-mobility group box 1 protein.
Article in Experimental and therapeutic medicine, 2018. 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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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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Who cites it
6 citing papers in PubMed, 8 citations in OpenAlex.
- Multimodal Mass Spectrometry Imaging of an Osteosarcoma Multicellular Tumour Spheroid Model to Investigate Drug-Induced Response.Metabolites · 2024Article
- RNA 5-methylcytosine status is associated with DNMT2/TRDMT1 nuclear localization in osteosarcoma cell lines.Journal of bone oncology · 2022Article
- miR-877-3p inhibits tumor growth and angiogenesis of osteosarcoma through fibroblast growth factor 2 signaling.Bioengineered · 2022Article
- Investigating Optimal Chemotherapy Options for Osteosarcoma Patients through a Mathematical Model.Cells · 2021Article
- Data-Driven Mathematical Model of Osteosarcoma.Cancers · 2021Article
- The Role of HMGB1, a Nuclear Damage-Associated Molecular Pattern Molecule, in the Pathogenesis of Lung Diseases.Antioxidants & redox signaling · 2019Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteosarcoma is among the commonly observed malignancies worldwide. High-mobility group box 1 protein (HMGB1) is a highly conserved protein and is involved in the progression of various types of human cancer. The aim of the present study was to explore whether the level of HMGB1 was involved in the necrosis of osteosarcoma cells. Doxorubicin (DXR), as an inducer of necrosis, was administered to human osteosarcoma cell lines (MG63, Saos-2 and U2OS), and the results indicated that 0.5 µg/ml DXR significantly induced the necrosis of MG63 cells (P<0.01), while 0.5 and 1.0 µg/ml DXR suppressed the viability of MG63 and U2OS cells (P<0.05), relative to untreated controls. Additionally, treatment with DXR was observed by western blot analysis to markedly increase the expression levels of HMGB1 in MG63 cells, and to significantly increase the levels of secreted HMGB1 in the supernatants of MG63 and U2OS cells (P<0.01). In conclusion, cell necrosis increased the level of HMGB1 in osteosarcoma cells, as well as the level of secreted HMGB1 in cell supernatants. Therefore, HMGB1 may be a potential target in molecular therapy for patients with osteosarcoma.
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