期刊
BMB REPORTS
卷 47, 期 4, 页码 227-232出版社
KOREAN SOCIETY BIOCHEMISTRY & MOLECULAR BIOLOGY
DOI: 10.5483/BMBRep.2014.47.4.128
关键词
Angiogenesis; Angiogenic factors; Anti cancer drug-resistance; Histone deacetylase-3; Tumor-induced angiogenesis
资金
- National Research Foundation [2010-0021357, 2011-0010867, 2012H1B8A202 5495, C1008749-01-01]
- National R&D Program for Cancer Control, Ministry for Health and Welfare, Republic of Korea [1320160]
- Kangwon National University [120131363]
- National Research Foundation of Korea [2010-0021357, 2011-0010867] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
Histone deacetylase-3 (HDAC3) is involved in cellular proliferation, apoptosis and transcriptional repression. However, the role of HDAC3 in angiogenesis remains unknown. HDAC3 negatively regulated the expression of angiogenic factors, such as VEGF and plasminogen activator inhibitor-1 (PAI-1). HDAC3 showed binding to promoter sequences of PAI-1. HDAC3 activity was necessary for the expression regulation of PAI-1 by HDAC3. VEGF decreased the expression of HDAC3, and the down-regulation of HDAC3 enhanced endothelial cell tube formation. HDAC3 negatively regulated tumor-induced angiogenic potential. We show the novel role of HDAC3 as a negative regulator of angiogenesis.
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