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

Figure 3.

Figure 3.

HDAC8 is required for SIRT7 transcriptional repression. (A) qRT-PCR analysis of SIRT7 in MDA-MB-231 cells treated with TGF-β1, NAM and TSA as indicated for 24 h. n.s, non-significant. The data represent the means ± s.e.m. n = 3, *P < 0.05, ***P < 0.001; Student's t-test. (B, C) SIRT7 levels were measured by qRT-PCR (B) and Immunoblotting (C) in HDAC6, HDAC8, HDAC10 and HDAC11 knocked down cells. The data represent the means ± s.e.m. n = 3, **P < 0.01; Student's t-test. (D) Immunoblotting analysis of SIRT7 level in cells incubated with the HDAC8 inhibitor PCI-34051 (PCI), in the presence or absence of TGF-β1 (5 ng/ml). (E, F) Immunoblotting (E) and qRT-PCR analysis (F) of SIRT7 expression in cells with ectopic HDAC8 over-expression. The data represent the means ± s.e.m. n = 3, ***P < 0.001; Student's t-test. (G) Luciferase assay of SIRT7 promoter activity with/without ectopic HDAC8 in the absence or presence of TGF-β1 (5 ng/ml). The data represent the means ± s.e.m.*P < 0.05; Student's t-test.