Title VEGF111b, a new member of VEGFxxxb isoforms and induced by mitomycin C, inhibits angiogenesis
Authors Gu, Fang
Li, Xiuli
Kong, Jian
Pan, Bing
Sun, Min
Zheng, Lemin
Yao, Yuanqing
Affiliation Chinese Peoples Liberat Army Gen Hosp, Dept Obstet & Gynecol, Beijing, Peoples R China.
Peking Univ, Inst Cardiovasc Sci,Hlth Minist, Key Lab Cardiovasc Mol Biol & Regulatory Peptides, Key Lab Mol Cardiovasc Sci,Educ Minist,Hlth Sci C, Beijing 100871, Peoples R China.
Peking Univ, Key Lab Cardiovasc Mol Biol & Regulatory Peptides, Sch Basic Med Sci,Educ Minist,Inst Syst Biomed, Key Lab Mol Cardiovasc Sci,Hlth Sci Ctr,Hlth Mini, Beijing 100871, Peoples R China.
Capital Med Univ, Beijing Chaoyang Hosp, Dept Hepatobiliary Surg, Beijing, Peoples R China.
Fourth Mil Med Univ, Tangdu Hosp, Dept Obstet & Gynecol, Xian 710032, Peoples R China.
Keywords VEGFxxxb
Anti-angiogenesis
Splice variant
VEGFR-2
ENDOTHELIAL GROWTH-FACTOR
SPLICE VARIANT
IN-VIVO
VEGF(165)B
NEOVASCULARIZATION
NEUROPILIN-1
VEGF(XXX)B
EXPRESSION
BINDING
PROTEIN
Issue Date 2013
Publisher 生物化学与生物物理学研究通讯
Citation BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS.2013,441,(1),18-24.
Abstract Vascular endothelial growth factor (VEGF-A) stimulating angiogenesis is required for tumor growth and progression. The conventional VEGF-A isoforms have been considered as pro-angiogenic factors. Another family of VEGF-A isoforms generated by alternative splicing, termed VEGFxxxb isoforms, has anti-angiogenic property, exemplified by VEGF165b. Here, we identify a new number of VEGFxxx family-VEGF111b induced by mitomycin C, although not detected in mitomycin C-unexposed ovarian cancer cells. SKOV3 cells were transfected with pcDNA(3.1) empty vector, pcDNA(3.1)-VEGF111b or pcDNA(3.1)-VEGF165b to collect conditioned mediums respectively. VEGF111b overexpression inhibits proliferation, migration and tube formation of endothelial cell by inhibiting VEGF-R2 phosphorylation and its downstream signaling, similar to VEGF165b but slightly lower than VEGF165b. The anti-angiogenic property depends on the six amino acids of exon 8b of the VEGFxxxb isoforms. Our results show that VEGF111b is a novel potent anti-angiogenic agent that can target the VEGF-R2 and its signaling pathway to inhibit ovarian tumor growth. (C) 2013 Elsevier Inc. All rights reserved.
URI http://hdl.handle.net/20.500.11897/220134
ISSN 0006-291X
DOI 10.1016/j.bbrc.2013.09.144
Indexed SCI(E)
Appears in Collections: 基础医学院
分子心血管学教育部重点实验室

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