Overexpression of platelet-derived growth factor-B increases the growth, invasion, and angiogenesis of gastric carcinoma cells through protein kinase B

Abstract

Platelet-derived growth factor-B (PDGF-B) promotes tumor metastasis by inducing tumor cell growth, invasion, and angiogenesis in several cancers. However, the roles of PDGF-B in gastric carcinoma are largely unknown. We established two gastric carcinoma cell lines, SGC7901 and BGC823, to stably overexpress PDGF-B by lentiviral vectors, and determined their growth, invasion and angiogenesis. Overexpression of PDGF-B significantly enhanced the cell proliferation, invasion and angiogenesis of both SGC7901 and BGC823 cells, accompanied with increased activation of AKT, which is a downstream target of PDGF signaling pathway. Consequently, an AKT kinase inhibitor abolished the PDGF-B overexpression-mediated up-regulation of growth, invasion and angiogenesis. These results indicate that PDGF-B signaling may promote the metastasis of gastric carcinoma through AKT signaling. Targeting the PDGF-B pathway may be an alternative strategy for the development of therapies for gastric cancers.