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  4. HDAC inhibition upregulates the expression of angiostatic ADAMTS1
 
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HDAC inhibition upregulates the expression of angiostatic ADAMTS1

Journal
FEBS Letters
Journal Volume
582
Journal Issue
29
Pages
4059-4065
Date Issued
2008
Author(s)
Chou C.-W.
CHING-CHOW CHEN  
DOI
10.1016/j.febslet.2008.10.048
URI
https://scholars.lib.ntu.edu.tw/handle/123456789/560415
Abstract
HDAC inhibitors are promising anticancer agents that induce cell cycle arrest and apoptosis. However, the role of HDACs in cancer progression, such as angiogenesis and metastasis, remains largely unexplored. Among various HDAC inhibitors, we demonstrate that TSA and SAHA upregulated the expression of angiostatic ADAMTS1 in A549 cells. HDAC6 inhibitor tubacin, and knockdown of HDAC6, also lead to ADAMTS1 upregulation. By reporter, DAPA, and ChIP assays, the proximal GC boxes were demonstrated to be essential for ADAMTS1 induction. Decreased binding of SP1 and HDAC6 to the ADAMTS1 promoter after TSA treatment was also seen. These data suggest the involvement of HDAC6 and SP1 in the HDACi-induced expression of angiostatic ADAMTS1. Crown Copyright ? 2008.
Subjects
ADAMTS1; HDAC6; SAHA; SP1; TSA
SDGs

[SDGs]SDG3

Other Subjects
histone deacetylase inhibitor; niltubacin; trichostatin A; tubacin; unclassified drug; von Willebrand factor cleaving proteinase; vorinostat; article; controlled study; enzyme inhibition; GC rich sequence; human; human cell; priority journal; promoter region; protein binding; protein expression; protein induction; upregulation
Type
journal article

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