ArticleJournal of orthopaedic surgery and research2010
Role of the VEGF-Flt-1-FAK pathway in the pathogenesis of osteoclastic bone destruction of giant cell tumors of bone.
Article in Journal of orthopaedic surgery and research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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10 citing papers in PubMed, 18 citations in OpenAlex.
- Recent topics in diagnosis and treatment of malignant spinal tumors.Fukushima journal of medical science · 2025Review
- Pharmacoproteogenomic approach identifies on-target kinase inhibitors for cancer drug repositioning.In vitro cellular & developmental biology. Animal · 2024Article
- Nuclear β-catenin translocation plays a key role in osteoblast differentiation of giant cell tumor of bone.Scientific reports · 2022Article
- Serglycin induces osteoclastogenesis and promotes tumor growth in giant cell tumor of bone.Cell death & disease · 2021Article
- Retrospective analysis of 51 intralesionally treated cases with progressed giant cell tumor of the bone: local adjuvant use of hydrogen peroxide reduces the risk for tumor recurrence.World journal of surgical oncology · 2019Article
- Expression of ezrin, CD44, and VEGF in giant cell tumor of bone and its significance.World journal of surgical oncology · 2015Article
- Differential Expression of ADAM23, CDKN2A (P16), MMP14 and VIM Associated with Giant Cell Tumor of Bone.Journal of Cancer · 2015Article
- Angiotensin-(1-7) attenuates metastatic prostate cancer and reduces osteoclastogenesis.The Prostate · 2013Article
- Evaluation of a biodegradable graft substitute in rabbit bone defect model.Indian journal of orthopaedics · 2012Article
- Systemic therapy for selected skull base sarcomas: Chondrosarcoma, chordoma, giant cell tumour and solitary fibrous tumour/hemangiopericytoma.Reports of practical oncology and radiotherapy : journal of Greatpoland Cancer Center in Poznan and Polish Society of Radiation OncologyReview
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11 authors at 1 institution in 1 country.
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Abstract
backgroundGiant cell tumors (GCTs) of bone are primary benign bone tumors that are characterized by a high number of osteoclast-like multinuclear giant cells (MNCs). Recent studies suggest that the spindle-shaped stromal cells in GCTs are tumor cells, while monocyte-like cells and MNCs are reactive osteoclast precursor cells (OPCs) and osteoclasts (OCs), respectively. In this study, we investigated the pathogenesis of osteoclastic bone destruction in GCTs by focusing on the role of the vascular endothelial growth factor (VEGF)-Flt-1 (type-1 VEGF receptor)-focal adhesion kinase (FAK) pathway.
methodsThe motility of OPCs cells was assessed by a chemotaxis assay and the growth of OPCs was examined using a cell proliferation assay. The expression of VEGF and activation of Flt-1 and FAK in clinical GCT samples and in OPCs were detected by immunohistochemistry and immunoblotting. The correlation between the expression levels of activated Flt-1 and FAK and clinical stages of GCTs was investigated by immunohistochemistry.
resultsIn GCT samples, CD68, a marker of OPCs and OCs, co-localized with Flt-1. Conditioned media from GCT tissue (GCT-CM) enhanced the chemotaxis and proliferation of OPCs. GCT-CM also stimulated FAK activation in OPCs in vitro. Moreover, there was a correlation between the clinical stage of GCTs and the expression of tyrosine-phosphorylated Flt-1 and FAK.
conclusionsOur results suggest that the VEGF-Flt-1-FAK pathway is involved in the pathogenesis of bone destruction of GCTs.
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