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    Butyrate histone deacetylase inhibitors.

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    License
    Attribution 4.0 International
    Date Issued
    2012-08
    Publisher Version
    10.1089/biores.2012.0223
    Author(s)
    Steliou, Kosta
    Boosalis, Michael S.
    Perrine, Susan P.
    Sangerman, José
    Faller, Douglas V.
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    Permanent Link
    https://hdl.handle.net/2144/40827
    Version
    Published version
    Citation (published version)
    Kosta Steliou, Michael S Boosalis, Susan P Perrine, José Sangerman, Douglas V Faller. 2012. "Butyrate histone deacetylase inhibitors.." Biores Open Access, Volume 1, Issue 4, pp. 192 - 198. https://doi.org/10.1089/biores.2012.0223
    Abstract
    In addition to being a part of the metabolic fatty acid fuel cycle, butyrate is also capable of inducing growth arrest in a variety of normal cell types and senescence-like phenotypes in gynecological cancer cells, inhibiting DNA synthesis and cell growth in colonic tumor cell lines, suppressing hTERT mRNA expression and telomerase activity in human prostate cancer cells, and inducing stem cell differentiation and apoptosis by DNA fragmentation. It regulates gene expression by inhibiting histone deacetylases (HDACs), enhances memory recovery and formation in mice, stimulates neurogenesis in the ischemic brain, promotes osteoblast formation, selectively blocks cell replication in transformed cells (compared to healthy cells), and can prevent and treat diet-induced obesity and insulin resistance in mouse models of obesity, as well as stimulate fetal hemoglobin expression in individuals with hematologic diseases such as the thalassemias and sickle-cell disease, in addition to a multitude of other biochemical effects in vivo. However, efforts to exploit the potential of butyrate in the clinical treatment of cancer and other medical disorders are thwarted by its poor pharmacological properties (short half-life and first-pass hepatic clearance) and the multigram doses needed to achieve therapeutic concentrations in vivo. Herein, we review some of the methods used to overcome these difficulties with an emphasis on HDAC inhibition.
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    Attribution 4.0 International
    Collections
    • MED: Medicine Papers [241]
    • BU Open Access Articles [3866]


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