A concise review of VEGF, PDGF, FGF, Notch, angiopoietin, and HGF signalling in tumor angiogenesis with a focus on alternative approaches and future directions

Abstract

Angiogenesis forms new vessels from existing ones. Abnormal angiogenesis, which is what gives tumor microenvironments their distinctive features, is characterised by convoluted, permeable blood vessels with a variety of shapes and high perfusion efficiency. Tumor angiogenesis controls cancer growth by allowing invasion and metastasis and is highly controlled by signalling networks. Therapeutic techniques targeting VEGF, PDGF, FGF Notch, Angiopoietin, and HGF signalling restrict the tumor's vascular supply. Numerous pathways regulate angiogenesis, and when one of those processes is blocked, the other pathways may step in to help. VEGF signalling inhibition alone has limits as an antiangiogenic therapy, and additional angiogenic pathways such as FGF, PDGF, Notch, angiopoietin, and HGF are important. For the treatment of advanced solid tumors, there are also new, emerging medicines that target multiple angiogenic pathways. Recent therapies block numerous signalling channels concurrently. This study focuses on ‘alternative’ methods to standard antiangiogenic medicines, such as cyclooxygenase-2 blocking, oligonucleotide binding complementary sites to noncoding RNAs to regulate mRNA target, matrix metalloproteinase inhibition and CRISPR/Cas9 based gene edition and dissecting alternative angiogenesis mechanism in tumor microenvironment.