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) |
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Pages (from-to) | 159-169 |
Number of pages | 11 |
Journal | Cancer Letters |
Volume | 333 |
Issue number | 2 |
DOIs | |
State | Published - Jun 10 2013 |
Keywords
- Angiogenesis
- FGF2
- Methylation
- MiR-503
- VEGFA
ASJC Scopus subject areas
- Oncology
- Cancer Research