ArticleBiomedicines2021
FAK Regulates VEGFR2 Expression and Promotes Angiogenesis in Triple-Negative Breast Cancer.
Article in Biomedicines, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 45 citations in OpenAlex.
- Non-receptor tyrosine kinase signaling pathways and therapeutic implications.Signal transduction and targeted therapy · 2026Review
- Vascular Endothelial Growth Factor Receptor 2 (VEGFR2/KDR) Promotes KSHV Lytic Replication and Drives Pro-Inflammatory Cytokine Release and Cancer Signaling.Journal of medical virology · 2026Article
- FAK inhibitor suppresses ovarian cancer growth by inhibiting tumor angiogenesis.Cancer cell international · 2026Article
- Focal adhesion kinase inhibition enhances response to checkpoint immunotherapy in hepatocellular carcinoma.Journal of translational internal medicine · 2026Article
- Melatonin inhibits FAK signaling to suppress PD-L1 expression and enhance chemosensitivity in triple-negative breast cancer.International journal of medical sciences · 2026Article
- Hemodynamic Inflow-Outflow Profiling as an Integrated DCE-MRI Biomarker for Diagnosis and Risk Stratification in Breast Cancer: A Multicenter Retrospective Study.Breast cancer (Dove Medical Press) · 2026Article
- Vascular endothelial generating factor pathway in ovarian cancer.Journal of ovarian research · 2025Review
- 3D In Vitro Models of Breast Cancer: Current Challenges and Future Prospects Toward Recapitulating the Microenvironment and Mimicking Key Processes.Advanced biology · 2025Review
- Pro-Angiogenic Bioactive Molecules in Vascular Morphogenesis: Integrating Endothelial Cell Dynamics.Current issues in molecular biology · 2025Review
- Strain Promotes Triple Negative Breast Cancer Proliferation and Migration Via VEGFR-2.Cellular and molecular bioengineering · 2025Article
- Multiscale computational evaluation of Vitex trifolia phytochemicals as VEGFR2 inhibitors for targeted breast cancer therapy.PloS one · 2025Article
- Zebrafish xenografts in breast cancer research.Frontiers in immunology · 2025Review
- Host angiogenic reprogramming byFrontiers in microbiology · 2025Article
- Ginsenoside potential targeting hypoxia-inducible factor-1α as promising therapeutics for cancer: a review.Frontiers in medicine · 2025Review
- Discovery of dual kinase inhibitors targeting VEGFR2 and FAK: structure-based pharmacophore modeling, virtual screening, and molecular docking studies.BMC chemistry · 2024Article
- Design, Synthesis and Biological Assessment ofPharmaceuticals (Basel, Switzerland) · 2024Article
- Vinorelbine Improves the Efficacy of Sorafenib against Hepatocellular Carcinoma: A Promising Therapeutic Approach.International journal of molecular sciences · 2024Article
- Roles and inhibitors of FAK in cancer: current advances and future directions.Frontiers in pharmacology · 2024Review
- Review
- Recent advances in targeted strategies for triple-negative breast cancer.Journal of hematology & oncology · 2023Review
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Triple-negative breast cancer (TNBC) remains a significant clinical challenge because of its high vascularity and metastatic and recurrent rates. Tumor angiogenesis is considered an important mediator in the regulation of tumor cell survival and metastasis in TNBC. Angiogenesis is induced by the binding of vascular endothelial growth factor to vascular endothelial growth factor receptor 2 (VEGFR2). Focal adhesion kinase (FAK) plays an important role in regulating various cell functions in normal and cancer cells. Previous studies have focused on investigating the function of endothelial FAK in tumor cell angiogenesis. However, the association between tumor FAK and VEGFR2 in tumor angiogenesis and the possible mechanisms of this remain unclear. In this study, we used a public database and human specimens to examine the association between FAK and VEGFR2. At the same time, we verified the association between FAK and VEGFR2 through several experimental methods, such as quantitative real-time polymerase chain reaction, Western blotting, and next-generation sequencing. In addition, we used the endothelial cell model, zebrafish, and xenograft animal models to investigate the role of FAK in TNBC angiogenesis. We found that FAK and VEGFR2 were positively correlated in patients with TNBC. VEGFR2 and several other angiogenesis-related genes were regulated by FAK. In addition, FAK regulated VEGFR2 and VEGF protein expression in TNBC cells. Functional assays showed that FAK knockdown inhibited endothelial tube formation and zebrafish angiogenesis. An animal model showed that FAK inhibitors could suppress tumor growth and tumor vascular formation. FAK promotes angiogenesis in TNBC cells by regulating VEGFR2 expression. Therefore, targeting FAK could be another antiangiogenic strategy for TNBC treatment.
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