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Background  Angiogenesis is the formation of neovasculature from a pre-existing vascular network. Progression of solid tumors including lung cancer is angiogenesis-dependent. We previously introduced a bioinformatics-based methodology to identify endogenous anti-angiogenic peptide sequences, and validated these predictions  in vitro  in human umbilical vein endothelial cell (HUVEC) proliferation and migration assays.    Methods  One family of peptides with high activity is derived from the α-fibrils of type IV collagen. Based on the results from the  in vitro  screening, we have evaluated the ability of a 20 amino acid peptide derived from the α5 fibril of type IV collagen, pentastatin-1, to suppress vessel growth in an angioreactor-based directed  in vivo  angiogenesis assay (DIVAA). In addition, pentastatin-1 suppressed tumor growth with intraperitoneal peptide administration in a small cell lung cancer (SCLC) xenograft model in nude mice using the NCI-H82 human cancer cell line.    Results  Pentastatin-1 decreased the invasion of vessels into angioreactors  in vivo  in a dose dependent manner. The peptide also decreased the rate of tumor growth and microvascular density  in vivo  in a small cell lung cancer xenograft model.    Conclusions  The peptide treatment significantly decreased the invasion of microvessels in angioreactors and the rate of tumor growth in the xenograft model, indicating potential treatment for angiogenesis-dependent disease, and for translational development as a therapeutic agent for lung cancer.

Pentastatin-1, a collagen IV derived 20-mer peptide, suppresses tumor growth in a small cell lung cancer xenograft model