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|Title:||Low arsenite concentrations induce cell proliferation via activation of VEGF signaling in human neuroblastoma SH-SY5Y cells|
Chulabhorn Research Institute
Chulabhorn Graduate Institute
|Keywords:||Environmental Science;Pharmacology, Toxicology and Pharmaceutics|
|Citation:||Environmental Toxicology and Pharmacology. Vol.33, No.1 (2012), 53-59|
|Abstract:||Arsenic widely contaminates the environment, especially in drinking water. Although it is a known carcinogen in humans, its carcinogenic mechanism has not yet been clarified. Here, we demonstrated that a low concentration of arsenite treatment induced proliferation of human neuroblastoma SH-SY5Y cells as indicated by increases in cell viability and BrdU incorporation. Additionally, arsenite increased VEGF expression and secretion. Inhibition of VEGF-induced signaling by SU4312, the inhibitor of VEGF receptor 2 kinase, and by treatment with anti-VEGF antibody blocked arsenite-induced increases in cell proliferation. Moreover, arsenite caused activation of ERK, a key signaling molecule involved in cell proliferation, and this activation was attenuated by SU4312, suggesting that ERK activation contributes to VEGF-mediated cell proliferation induced by arsenite. Collectively, the present study reveals that a mechanism underlying arsenic-induced cell proliferation may be through induction and activation of VEGF signaling, and this may subsequently contribute to tumor formation. © 2011 Elsevier B.V.|
|Appears in Collections:||Scopus 2011-2015|
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