HDAC turnover, CtIP acetylation and dysregulated DNA damage signaling in colon cancer cells treated with sulforaphane and related dietary isothiocyanates.

3A ), with SFN, 6-SFN and 9-SFN being highly significant (p < 0.001).

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37 - 39 These findings may be significant, because SFN-induced DNA damage is repaired predominantly through homologous recombination, 40 and destabilizing a critical repair protein in this pathway, CtIP, provides an avenue for synthetic lethality. 41 HDACs maintain CtIP in the deacetylated state, whereas GCN5-mediated acetylation shunts CtIP into autophagy-mediated degradation. 7 We observed that ITC-induced CtIP acetylation and turnover coincided with the activation of an autophagic response, the degree of which increased with length of the alkyl side chain ( Fig. 6 ).

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