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. 2020 Jan 23;48(6):2912–2923. doi: 10.1093/nar/gkaa039

Figure 5.

Figure 5.

HDAC8 inhibition attenuates TGF-β signaling. (A) SMAD4 protein levels in MDA-MB-231 breast cancer cells exposed to the indicated treatments. CHX, cycloheximide (50 μg/ml). (B, C) qRT-PCR analysis of TGF-β downstream genes in MDA-MB-231 breast cancer cells. The data represent the means ± s.e.m. n = 3, *P < 0.05, **P < 0.01, ***P < 0.001; Student's t-test. (D) A schematic model: (a) SIRT7 deacetylates SMAD4, leading to its degradation and ensuring basal activity of TGF-β signaling; (b) HDAC8 cooperates with SMAD3/4 heterotrimer to suppress SIRT7 transcription, causing hyperactivation of TGF-β signaling.