VEGF/VEGFR: A Novel Therapy Target in Cancer

Abstract: Angiogenesis reduction with VEGF/VEGFR (Vascular Endothelial Growth Factor/ Vascular Endothelial Growth Factor Receptor) inhibition is the target of our review. Angiogenesis is the development of blood vessels and affects cancer spread and progression. The angiogenesis process is triggered by a number of growth factors, including cytokines, VEGF, FGF (fibroblast growth factor), and PDGF (platelet-derived growth factor). VEGF and VEGFR are two factors that significantly impact the angiogenesis process. VEGFRs are Kinase Domain Receptors (KDRs). Upon activation, KDRs trigger autophosphorylation, which leads to tumor growth, metastasis, and cell proliferation. Numerous cancer types, including breast, renal, non-small cell lung, cervical, hepatocellular, and others, have been linked to overexpression of VEGFR. It has been established that VEGF/ VEGFR overexpression or gene amplification occurs in certain malignancies. Furthermore, an increasing amount of research has shown that blocking VEGF/VEGFR may enhance the effects of chemotherapy. In recent decades, several VEGF/VEGFR inhibitors have been developed that effectively inhibit the growth and progression of several malignancies in vivo and in vitro, suggesting that VEGF/VEGFR could be a novel target for therapeutic intervention. In this review, we started by quickly going over the composition, location, and physiological roles of VEGF/VEGFR during mitosis. The oncogenic function of VEGF/VEGFR in the development of cancer has then been covered. Lastly, we have discussed the prospective anticancer therapy provided by the clinically authorized VEGFR inhibitors.