ArticleCell death & disease2022
Bevacizumab attenuates osteosarcoma angiogenesis by suppressing MIAT encapsulated by serum-derived extracellular vesicles and facilitating miR-613-mediated GPR158 inhibition.
Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 19 citations in OpenAlex.
- Bevacizumab induces apoptosis in glioblastoma cells by upregulating miR-4695-5p to inhibit PKMYT1.RNA biology · 2026Article
- Tumor microenvironment-rearranging Nanoassemblies overcome angiogenesis-immunotherapy resistance to potentiate osteosarcoma treatment.Materials today. Bio · 2026Article
- Immunotherapy combined with anti-angiogenic therapy, radiotherapy and chemotherapy for the treatment of giant pelvic osteosarcoma: A case report and literature review.Oncology letters · 2026Article
- Extracellular vesicles in osteosarcoma: bridging resistance, immunity, and clinical translation.Journal of bone oncology · 2026Review
- Extracellular Vesicles in Osteosarcoma: Mechanisms, Diagnostics and Therapeutic Applications.Drug design, development and therapy · 2026Review
- Tumor microenvironment in osteosarcoma: From cellular mechanism to clinical therapy.Genes & diseases · 2025Review
- ROLE OF POLYMORPHISMS IN VEGF AND KDR GENES IN OSTEOSARCOMA SUSCEPTIBILITY: A SYSTEMATIC REVIEW.Acta ortopedica brasileira · 2025Review
- Vascular motion in the dorsal root ganglion sensed by Piezo2 in sensory neurons triggers episodic pain.Neuron · 2025Article
- The clinical and molecular landscape of breast cancer in women of African and South Asian ancestry.Nature communications · 2025Article
- Roles of lncRNA in the crosstalk between osteogenesis and angiogenesis in the bone microenvironment.Journal of Zhejiang University. Science. B · 2025Review
- Extracellular Vesicles in Sarcoma: Implications for Tumor Progression and Therapy.International journal of nanomedicine · 2025Review
- Osteocalcin and GPR158: linking bone and brain function.Frontiers in cell and developmental biology · 2025Review
- Functional Relevance of Extracellular Vesicle-Derived Long Non-Coding and Circular RNAs in Cancer Angiogenesis.Non-coding RNA · 2024Review
- Extracellular vesicles in tumorigenesis, metastasis, chemotherapy resistance and intercellular communication in osteosarcoma.Bioengineered · 2023Review
- The emerging roles of GPR158 in the regulation of the endocrine system.Frontiers in cell and developmental biology · 2022Review
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Targeting angiogenesis has been considered a promising treatment for a large number of malignancies, including osteosarcoma. Bevacizumab (Bev) is an anti-vascular endothelial growth factor being used for this purpose. We herein investigate the therapeutic potential of Bev in angiogenesis during osteosarcoma and the related mechanisms. Bioinformatics were performed for identification of osteosarcoma-related microarray dataset to collect related lncRNA and miRNA, with MIAT and miR-613 obtained. The predicted binding site between miR-613 and GPR158 3'UTR region was further confirmed by luciferase assay. Then, their effects combined with treatment with Bev on osteosarcoma cells were explored by the gain- and loss-of-function. After extraction from osteosarcoma patients' serum (serum-EVs) and identification, EVs were co-cultured with osteosarcoma cells, the biological behaviors of which were detected by CCK-8 assay and microtubule formation in vitro. A mouse tumor xenograft model was used to determine the effect of Bev on tumor angiogenesis in vivo. Bev inhibited osteosarcoma cell proliferation and angiogenesis in vivo and in vitro. Besides, serum-EVs could transfer MIAT (EV-MIAT) into osteosarcoma cells, where it is competitively bound to miR-613 to elevate GPR158, thus promoting osteosarcoma cell proliferation and angiogenesis. Furthermore, Bev arrested osteosarcoma cell proliferation and angiogenesis by inhibiting EV-MIAT and inducing miR-613-mediated GPR158 inhibition. In conclusion, the Bev-mediated MIAT/miR-613/GPR158 regulatory feedback revealed a new molecular mechanism in the pathogenesis of osteosarcoma angiogenesis.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.