Sodium butyrate inhibits c-myc splicing and interferes with signal transduction in ovarian carcinoma cells

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Abstract
Sodium butyrate (NaB), a physiologically produced short chain fatty acid, dramatically changes the growth rate and also the morphology of a fast growing subclone (N.1) derived from the heterogenous human ovarian carcinoma HOC-7. The mRNA of the growth related proto-oncogene c-myc, constitutively expressed in N.1 cells decreased significantly within 24 h of NaB treatment and remained suppressed until the NaB block was released. Down-regulation was accomplished partially by accelerating degradation of c-myc mRNA and by inhibiting splicing of c-myc transcripts. We demonstrated that NaB blocked general mechanisms in signal transduction, such as the release of Ca2+ from intracellular stores, and modulated the activity of serine/threonine kinases. The multiple effects of sodium butyrate on HOC-7 derivatives, as well as on a variety of other cell types investigated by others, may be due to interference with general mechanisms of signal transduction.