Figure 3.

Summary of key findings. In the Apc^min mouse, HDAC/co-repressor complexes maintain a tightly restricted chromatin configuration, which limits access of transcription factors to DNA, and represses genes required for cell cycle checkpoint control and apoptosis. Inhibition of HDAC by SFN enables acetyl groups (“ac”) to be added to histone tails, loosening DNA/chromatin interactions, and allowing access of transcription factors to the promoters of genes such as P21 and bax. Re-expression of these genes triggers cell cycle arrest and apoptosis in transformed cells and microadenomas, thereby suppressing polyp formation.