MicroRNA-503 targets FGF2 and VEGFA and inhibits tumor angiogenesis and growth

Bisheng Zhou; Ruihua Ma; Wenxia Si; Sisi Li; Yan Xu; Xin Tu; Qing Wang

doi:10.1016/j.canlet.2013.01.028

MicroRNA-503 targets FGF2 and VEGFA and inhibits tumor angiogenesis and growth

Bisheng Zhou, Ruihua Ma, Wenxia Si, Sisi Li, Yan Xu, Xin Tu, Qing Wang^*

^*Corresponding author for this work

Medicine, Pulmonary Division

Research output: Contribution to journal › Article › peer-review

174 Scopus citations

Abstract

FGF2 and VEGFA are the two most potent angiogenic factors. Here we report that miR-503 can simultaneously down-regulate FGF2 and VEGFA. The expression of miR-503 is repressed in HCC cells and primary tumors due to a potential epigenetic mechanism. Overexpression of miR-503 reduced tumor angiogenesis in vitro and in vivo. We also found that miR-503 expression was down-regulated by hypoxia through HIF1α. These results identify a miRNA that targets both FGF2 and VEGFA in cancers, demonstrate the anti-angiogenesis role of miR-503 in tumorigenesis, and provide a novel mechanism for hypoxia-induced FGF2 and VEGFA through HIF1α-mediated inhibition of miR-503.

Original language	English (US)
Pages (from-to)	159-169
Number of pages	11
Journal	Cancer Letters
Volume	333
Issue number	2
DOIs	https://doi.org/10.1016/j.canlet.2013.01.028
State	Published - Jun 10 2013

Funding

This work was supported by a National Basic Research (973) Program Grant ( 2013CB0531101 ), a Grant from the State Key Laboratory of Freshwater Ecology and Biotechnology ( 2011FB16 ), the Fundamental Research Funds for the Central Universities ( 2010MS015 ), and a Key Academic Program Leader Award of Wuhan City ( 200951830560 ).

Keywords

Angiogenesis
FGF2
Methylation
MiR-503
VEGFA

ASJC Scopus subject areas

Oncology
Cancer Research

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1016/j.canlet.2013.01.028

Cite this

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title = "MicroRNA-503 targets FGF2 and VEGFA and inhibits tumor angiogenesis and growth",

abstract = "FGF2 and VEGFA are the two most potent angiogenic factors. Here we report that miR-503 can simultaneously down-regulate FGF2 and VEGFA. The expression of miR-503 is repressed in HCC cells and primary tumors due to a potential epigenetic mechanism. Overexpression of miR-503 reduced tumor angiogenesis in vitro and in vivo. We also found that miR-503 expression was down-regulated by hypoxia through HIF1α. These results identify a miRNA that targets both FGF2 and VEGFA in cancers, demonstrate the anti-angiogenesis role of miR-503 in tumorigenesis, and provide a novel mechanism for hypoxia-induced FGF2 and VEGFA through HIF1α-mediated inhibition of miR-503.",

keywords = "Angiogenesis, FGF2, Methylation, MiR-503, VEGFA",

author = "Bisheng Zhou and Ruihua Ma and Wenxia Si and Sisi Li and Yan Xu and Xin Tu and Qing Wang",

note = "Funding Information: This work was supported by a National Basic Research (973) Program Grant ( 2013CB0531101 ), a Grant from the State Key Laboratory of Freshwater Ecology and Biotechnology ( 2011FB16 ), the Fundamental Research Funds for the Central Universities ( 2010MS015 ), and a Key Academic Program Leader Award of Wuhan City ( 200951830560 ). ",

year = "2013",

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doi = "10.1016/j.canlet.2013.01.028",

language = "English (US)",

volume = "333",

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journal = "Cancer Letters",

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T1 - MicroRNA-503 targets FGF2 and VEGFA and inhibits tumor angiogenesis and growth

AU - Zhou, Bisheng

AU - Ma, Ruihua

AU - Si, Wenxia

AU - Li, Sisi

AU - Xu, Yan

AU - Tu, Xin

AU - Wang, Qing

N1 - Funding Information: This work was supported by a National Basic Research (973) Program Grant ( 2013CB0531101 ), a Grant from the State Key Laboratory of Freshwater Ecology and Biotechnology ( 2011FB16 ), the Fundamental Research Funds for the Central Universities ( 2010MS015 ), and a Key Academic Program Leader Award of Wuhan City ( 200951830560 ).

PY - 2013/6/10

Y1 - 2013/6/10

N2 - FGF2 and VEGFA are the two most potent angiogenic factors. Here we report that miR-503 can simultaneously down-regulate FGF2 and VEGFA. The expression of miR-503 is repressed in HCC cells and primary tumors due to a potential epigenetic mechanism. Overexpression of miR-503 reduced tumor angiogenesis in vitro and in vivo. We also found that miR-503 expression was down-regulated by hypoxia through HIF1α. These results identify a miRNA that targets both FGF2 and VEGFA in cancers, demonstrate the anti-angiogenesis role of miR-503 in tumorigenesis, and provide a novel mechanism for hypoxia-induced FGF2 and VEGFA through HIF1α-mediated inhibition of miR-503.

AB - FGF2 and VEGFA are the two most potent angiogenic factors. Here we report that miR-503 can simultaneously down-regulate FGF2 and VEGFA. The expression of miR-503 is repressed in HCC cells and primary tumors due to a potential epigenetic mechanism. Overexpression of miR-503 reduced tumor angiogenesis in vitro and in vivo. We also found that miR-503 expression was down-regulated by hypoxia through HIF1α. These results identify a miRNA that targets both FGF2 and VEGFA in cancers, demonstrate the anti-angiogenesis role of miR-503 in tumorigenesis, and provide a novel mechanism for hypoxia-induced FGF2 and VEGFA through HIF1α-mediated inhibition of miR-503.

KW - Angiogenesis

KW - FGF2

KW - Methylation

KW - MiR-503

KW - VEGFA

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DO - 10.1016/j.canlet.2013.01.028

M3 - Article

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AN - SCOPUS:84876737342

SN - 0304-3835

VL - 333

SP - 159

EP - 169

JO - Cancer Letters

JF - Cancer Letters

IS - 2

ER -

MicroRNA-503 targets FGF2 and VEGFA and inhibits tumor angiogenesis and growth

Abstract

Funding

Keywords

ASJC Scopus subject areas

UN SDGs

Access to Document

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