Abstract
This chapter discusses the role of kinin peptides bradykinin (BK) in cancer growth. BK is a pluripotent factor for cancer growth. Many tumor types have mutated to stimulate increased production of BK and expression of BK receptors. These activities work together for autocrine stimulation of tumor growth. In tumors, BK stimulates growth directly and also stimulates neovascularization of tumors by stimulating release of vascular endothelial growth factor (VEGF). BK also facilitates tumor migration and invasion by stimulating release of matrix metalloproteases (MMP). The potent and enzyme-resistant BK antagonist B-9430 was found to inhibit BK-evoked increase in intracellular calcium concentration in small cell lung cancer (SCLC) cells in culture, but it did not inhibit cell growth. However, when B-9430 was cross-linked with a suberimide linker at the amino terminus, the resulting dimer, B-9870, also known as CU-201, was found to be a very potent stimulus for apoptosis in cultured SCLC, BK antagonists, both peptides and peptidomimetics, are under research as potential new anticancer drugs. They offer the unique potential of triple combination cancer chemotherapy with a single agent.
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