Journal
JOURNAL OF BIOMEDICAL NANOTECHNOLOGY
Volume 9, Issue 10, Pages 1746-1756Publisher
AMER SCIENTIFIC PUBLISHERS
DOI: 10.1166/jbn.2013.1678
Keywords
Gold Nanoparticles; NSOM; VEGFR2; Hepatic Cancer
Funding
- National Basic Research Program from the Ministry of Science and Technology of China [2010CB833603]
- National Natural Science Foundation of China [30772131, 31201028]
- Natural Science Foundation of Guangdong Province [8151063201000034, S2011040003278]
- First Affiliated Hospital of Jinan University Scientific Foster Fund [511005004]
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The inhibition of the binding between VEGFs and their receptors reduces angiogenesis and retards tumor growth. Owing to the large amount of antibodies required, the antibody-based anti-angiogenic drug remains limited. Gold nanoparticles (AuNPs) displayed excellent biocompatibility, low toxicity and anti-angiogenic effect, but the mechanism of anti-angiogenesis was unknown. Here, the antitumor effects of a well-dispersed AuNPs, specifically regarding its influence on VEGF signaling, were examined mechanistically. The effects of AuNPs on the interaction of VEGF with its receptor, VEGFR2 were observed using near-field scanning optical microscopy/quantum dot (NSOM/QD) imaging. We found AuNPs can reduce VEGF(165)-induced VEGFR2 and AKT phosphorylation. Furthermore, the antitumor effects of AuNPs were determined using xenograft and ascites model. AuNPs inhibited VEGF(165)-VEGFR2 interaction and suppressed the formation of nanodomains of VEGFR2 on the HUVEC. As determined by CD34 immunhistochemistry, AuNPs reduced angiogenesis in a liver tumor nude mice model, as observed by a decreased microvascular density in liver tumor sections and reduced the tumor weight and volume. In addition, AuNPs inhibited ascites formation in mice. Taken together, this study provides new insights into nanomaterial-based antitumor drug development.
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