Activation of the γ-glutamyltransferase promoter 2 in the rat colon carcinoma cell line CC531 by histone deacetylase inhibitors is mediated through the Sp1 binding motif

Histone deacetylase inhibitors induce FPGS mRNA expression and intracellular accumulation of long-chain methotrexate polyglutamates in childhood acute lymphoblastic leukemia: implications for combination therapy

“…55,57 Histone deacetylase-1 inhibitors have been shown to enhance the transcription activity of promoters in a variety of cellular and viral genes containing Sp1-binding sites. [58][59][60][61][62] Sp1 belongs to the Sp family of transcription factors (Sp1-Sp4) that bind to the same consensus sequences (GGGCGG). 63 As other factors can also interact with Sp1, competition between transcription factors and HDACs may represent a general way to regulate gene expression via reversible modifications of chromatin structure.…”

An Sp1 Response Element in the Kaposi's Sarcoma-Associated Herpesvirus Open Reading Frame 50 Promoter Mediates Lytic Cycle Induction by Butyrate

“…The human insulin-like growth factor binding protein 3 promoter is activated via Sp1 sites in cells from breast cancer (79). In murine and rat cells, the Sp1 site has been found to be important in induction of the promoters of the gamma glutamyl transferase, nonmuscle myosin heavy chain II-3, and galectin genes (6,36,45). Butyrate is known to cause hyperacetylation of the tails of histones H3 and H4 in many cell types, including Friend leukemia cells, HeLa cells from cervical carcinoma, and CoCa from colon carcinoma (14).…”

Concurrent opposite effects of trichostatin A, an inhibitor of histone deacetylases, on expression of α-MHC and cardiac tubulins: implication for gain in cardiac muscle contractility

“…Whether EGR-1/ Sp-1 competition occurs on the ␣-MHC gene promoter is not known. However, if it does, it will be relevant in explaining the transactivation effect of EGR-1 by changing the activity of Sp1, which has been shown to be responsive to HDAC inhibition leading to gene activation (30,45). In the present study, by utilizing several additional approaches, including the protein-DNA array, transcription reporter array, cotransfection assays, heterologous promoter-reporter assays, and Western analyses, we concluded that overall TSA-mediated upregulation of EGR-1 expression is necessary for the activation of ␣-MHC gene expression.…”