ArticleNeoplasia (New York, N.Y.)2018
CXCR2-Expressing Tumor Cells Drive Vascular Mimicry in Antiangiogenic Therapy-Resistant Glioblastoma.
Article in Neoplasia (New York, N.Y.), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 68 citations in OpenAlex.
- The Significance of CXCL1 in Cancer: An Overview of Molecular Mechanisms.International journal of molecular sciences · 2026Review
- Crosstalk in the brain tumor microenvironment: mechanisms, therapeutic strategies, and clinical advances.Military Medical Research · 2026Review
- The presence of persistent synovial inflammation after "Eradication" unmasks the "Unseen" dormant state of infection allowing the prediction of infection free survival in total joint replacements.Journal of translational medicine · 2025Article
- ERα-dependent crosstalk between macrophages and cancer cells potentiates vasculogenic mimicry and M2 macrophage polarization in bladder cancer.Cell communication and signaling : CCS · 2025Article
- Pleiotrophin promote glioma proliferation and invasion by enhancing NF-κB/SLUG mediated epithelial-mesenchymal transition.European journal of medical research · 2025Article
- Review
- Hyperlipidemia-associated specific modules and hub genes revealed by integrative methods of WGCNA and MetaDE.Frontiers in genetics · 2025Article
- Vascular mimicry as a facilitator of melanoma brain metastasis.Cellular and molecular life sciences : CMLS · 2024Article
- The Clinical Significance and Involvement in Molecular Cancer Processes of Chemokine CXCL1 in Selected Tumors.International journal of molecular sciences · 2024Review
- Mechanisms of angiogenesis in tumour.Frontiers in oncology · 2024Review
- Review
- Vascular co-option and vasculogenic mimicry mediate resistance to antiangiogenic strategies.Cancer reports (Hoboken, N.J.) · 2022Review
- Current perspectives on diffuse midline glioma and a different role for the immune microenvironment compared to glioblastoma.Journal of neuroinflammation · 2022Review
- Glioblastoma-Specific Strategies of Vascularization: Implications in Anti-Angiogenic Therapy Resistance.Journal of personalized medicine · 2022Review
- Combining TMZ and SB225002 induces changes of CXCR2 and VEGFR signalling in primary human endothelial cellsOncology reports · 2022Article
- The emerging roles of circular RNAs in vessel co-option and vasculogenic mimicry: clinical insights for anti-angiogenic therapy in cancers.Cancer metastasis reviews · 2022Review
- Friends with Benefits: Chemokines, Glioblastoma-Associated Microglia/Macrophages, and Tumor Microenvironment.International journal of molecular sciences · 2022Review
- CXCR2 Receptor: Regulation of Expression, Signal Transduction, and Involvement in Cancer.International journal of molecular sciences · 2022Review
- Tumour-associated CD204Neuropathology and applied neurobiology · 2022Article
- EBV-Induced CXCL8 Upregulation Promotes Vasculogenic Mimicry in Gastric CarcinomaFrontiers in cellular and infection microbiology · 2022Article
Corrections and comments
- Erratum issued
Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundGlioblastoma (GBM) was shown to relapse faster and displayed therapeutic resistance to antiangiogenic therapies (AATs) through an alternative tumor cell-driven mechanism of neovascularization called vascular mimicry (VM). We identified highly upregulated interleukin 8 (IL-8)-CXCR2 axis in tumor cells in high-grade human glioma and AAT-treated orthotopic GBM tumors.
methodsHuman GBM tissue sections and tissue array were used to ascertain the clinical relevance of CXCR2-positive tumor cells in the formation of VM. We utilized U251 and U87 human tumor cells to understand VM in an orthotopic GBM model and AAT-mediated enhancement in VM was modeled using vatalanib (anti-VEGFR2) and avastin (anti-VEGF). Later, VM was inhibited by SB225002 (CXCR2 inhibitor) in a preclinical study.
resultsOverexpression of IL8 and CXCR2 in human datasets and histological analysis was identified as a bonafide candidate to validate VM through in vitro and animal model studies. AAT-treated tumors displayed a higher number of CXCR2-positive GBM-stem cells with endothelial-like phenotypes. Stable knockdown of CXCR2 expression in tumor cells led to decreased tumor growth as well as incomplete VM structures in the animal models. Similar data were obtained following SB225002 treatment.
conclusionsThe present study suggests that tumor cell autonomous IL-8-CXCR2 pathway is instrumental in AAT-mediated resistance and VM formation in GBM. Therefore, CXCR2 can be targeted through SB225002 and can be combined with standard therapies to improve the therapeutic outcomes in clinical trials.
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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.