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Arsenic trioxide (As 2 O 3 ) exhibits a remarkable effect on leukemia treatment; however, its effect on solid tumors remains poorly explored. The present study demonstrated the inhibitory effect of As 2 O 3 on lung cancer and explored its possible mechanism. It was observed that As 2 O 3 significantly inhibited the growth of lung cancer xenografts and tumor angiogenesis in vivo . The inhibitory effect of As 2 O 3 on cell proliferation in vitro was more remarkable in vascular endothelial cells than in lung cancer cells. It was also observed that As 2 O 3 inhibited the migration of vascular endothelial cells and disrupted vascular tube formation on Matrigel assays. In addition, a series of key signaling factors involved in multiple stages of angiogenesis, including matrix metalloproteinase (MMP)-2, MMP-9, platelet-derived growth factor (PDGF)-BB/PDGF receptor-β, vascular endothelial growth factor (VEGF)-A/VEGF receptor-2, basic fibroblast growth factor (FGF)/FGF receptor-1 and delta like canonical Notch ligand 4/Notch-1, were regulated by As 2 O 3 . These findings suggested that anti-angiogenesis may be an underlying mechanism of As 2 O 3 anticancer activity in lung cancer.

Anti-angiogenic effect of arsenic trioxide in lung cancer via inhibition of endothelial cell migration, proliferation and tube formation