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  • Title: [Molecular mechanism of inhibition of sodium butyrate on activation of tumor associated aromatase promoters].
    Author: Zhou JF, Liu WL, Chen G, Lu YP, Ma D.
    Journal: Ai Zheng; 2002 Dec; 21(12):1283-7. PubMed ID: 12520731.
    Abstract:
    BACKGROUND & OBJECTIVE: Sodium butyrate, a histone deacetylase inhibitor, can inhibit tumor conditioned medium-induced levels of promoter II and I. 3-specific transcripts. This study was designed to investigate the action of sodium butyrate on promoter II and I. 3 activity, which can be directed to elucidation of local estrogen production in breast cancer. METHODS: Primary human adipose fibroblasts (HAF) treated with MCF-7 breast cancer cell-conditioned medium were used as a cell model system. Promoter II and I. 3 deletion luciferase constructs was transfected into HAF. Western blotting and electrophoretic mobility shift assay were performed to evaluate the effect of sodium butyrate on promoter II and I .3. RESULTS: Breast cancer cell-conditioned medium enhanced phosphorylation of activator transcription factor-2 (ATF-2) which was the main modulatory subtype in CREB/ATF-2 family. The effect of sodium butyrate on aromatase expression in breast tumor fibroblasts was mediated by inhibition of phosphorylation of ATF-2, and hence, the inhibition of binding of a transcriptional complex containing phosphorylated ATF-2, C/EBP beta and CREB binding protein (CBP) to promoter II/I. 3 regulatory region. CONCLUSIONS: Sodium butyrate reduces the level of aromatase mRNA arising from cancer-induced promoter region. The aberrant activation of promoter II and I. 3 in HAF is dependent on the phosphorylation of ATF-2.
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