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. 2019 May 3;18(1):339–347. doi: 10.3892/ol.2019.10309

Figure 4.

Figure 4.

HDAC1 overexpression upregulates vimentin expression via the NF-κB signaling pathway. (A) Chromatin immunoprecipitation assay using an anti-p65 antibody to detect NF-κB binding to vimentin promoter. (B) THLE-3 cells were mock transfected or transfected with control siRNA or p65 siRNA and p65 expression was determined by western blotting. (C) THLE-3 cells were treated with p65 siRNA or control siRNA, and were further transfected with (−800/+72) Vimentin together with or without HDAC1 and the luciferase activity was measured. ns, not significant; *P<0.05, ***P<0.001. (D) THLE-3 cells were first transfected with (−800/+72) Vimentin together with sham vector or a combination of p65 and p50 and the luciferase activity was measured. **P<0.01 vs. pcDNA3.1. (E) THLE-3 cells were transfected with (−800/+72) Vimentin with or without HDAC1 for 4–6 h, then treated with NF-κB or JNK signaling pathway inhibitors and the luciferase activity was measured. ns, not significant; ***P<0.001. HDAC1, histone deacetylase 1; NF-κB, nuclear factor κ-light-chain-enhancer of activated B cells; p50, NF-κB p105 subunit; p65, transcription factor p65; siRNA, small interfering RNA.