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HERO ID
7064767
Reference Type
Journal Article
Title
Anlotinib inhibits angiogenesis via suppressing the activation of VEGFR2, PDGFRβ and FGFR1
Author(s)
Lin, B; Song, X; Yang, D; Bai, D; Yao, Y; Lu, N; ,
Year
2018
Is Peer Reviewed?
Yes
Journal
Gene
ISSN:
0378-1119
EISSN:
1879-0038
Publisher
ELSEVIER SCIENCE BV
Location
AMSTERDAM
Page Numbers
77-86
Language
English
PMID
29454091
DOI
10.1016/j.gene.2018.02.026
Web of Science Id
WOS:000429393900011
Abstract
Tumor cells recruit vascular endothelial cells and circulating endothelial progenitor cells to form new vessels to support their own growth and metastasis. VEGF, PDGF-BB and FGF-2 are three major pro-angiogenic factors and applied to promote angiogenesis. In this research, we demonstrated that anlotinib, a potent multi-tyrosine kinases inhibitor (TKI), showed a significant inhibitory effect on VEGF/PDGF-BB/FGF-2-induced angiogenesis in vitro and in vivo. Wound healing assay, chamber directional migration assay and tube formation assay indicated that anlotinib inhibited VEGF/PDGF-BB/FGF-2-induced cell migration and formation of capillary-like tubes in endothelial cells. Furthermore, anlotinib suppressed blood vessels sprout and microvessel density in rat aortic ring assay and chicken chorioallantoic membrane (CAM) assay. Importantly, according to our study, the anti-angiogenic effect of anlotinib is superior to sunitinib, sorafenib and nintedanib, which are three main anti-angiogenesis drugs in clinic. Mechanistically, anlotinib inhibits the activation of VEGFR2, PDGFRβ and FGFR1 as well their common downstream ERK signaling. Therefore, anlotinib is a potential agent to inhibit angiogenesis and be applied to tumor therapy.
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