Τόμος 23 (2009) – Τεύχος 3 – Άρθρο 3 – Επιθεώρηση Κλινικής Φαρμακολογίας και Φαρμακοκινητικής-Διεθνής Έκδοση – Volume 23 (2009) – Issue 3 – Article 3 – Epitheorese Klinikes Farmakologias και Farmakokinetikes-International Edition

Title Sodium butyrate: a deacetylase inhibitor with potential antineoplastic effect in monotherapy or in combination
Authors S. Massouridou1, H. Frangou1 and E.-N. Emmanouil-Nikoloussi2

1. Department of General Biology, Medical School and 2. Laboratory of Histology-Embryology and Anthropology, Aristotle University, Thessaloniki, Hellas

Citation Massouridou, S., Frangou, H., Emmanouil-Nikoloussi, E.-N.: Sodium butyrate: a deacetylase inhibitor with potential antineoplastic effect in monotherapy or in combination, Epitheorese Klin. Farmakol. Farmakokinet. 23(3): 125-130 (2009)
Publication Date Accepted for publication (Final Version): July 1, 2009
Full Text Language English
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Keywords Sodium butyrate, NaBu, apoptosis, anticancer drug, cytotoxic agents, anticancer drug, plasminogen, histone deacetylase inhibitors, histone modification.
Other Terms review article
Summary Sodium butyrate (NaBu) a naturally occurring short-chain fatty acid that is byproduct of carbohydrate metabolism in the gut, is one of the most widely studied histone deacetylase inhibitors HDIs (Histone Deacetylase Inhibitors). NaBu induces cell cycle arrest, differentiation, and apoptosis in some human tumor cell lines. HDIs are emerging as a promising new class of chemotherapeutic agents. HDIs, are in evidence as a potential new class of antineoplastic agents because they are able to promote or enhance a variety of different anticancer mechanisms, including apoptosis, cell cycle arrest and cellular differentiation. HDIs function by inhibiting histone deacetylases, resulting in the accumulation of acetylated histones, in turn leading to an increase in transcriptionally active chromatin. They reactivate gene expression of dormant tumour suppressor genes such as CDKN1A (p21) and modulates the expression of a large number of genes. Beside their direct anti-tumor activity HDIs also enhance the cytotoxic effects of some therapeutic regimens like ionizing radiation, chemotherapy and recombinant tumor necrosis factor-related apoptosis-inducing ligand (TRAIL). Therefore, the use of HDIs in association with classical chemotherapeutic drugs or in combination with DNA demethylating agents could be a promising treatment alternative.
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