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. 2018 May 24;31:276–286. doi: 10.1016/j.ebiom.2018.05.003

Fig. 5.

Fig. 5

WW437 significantly inhibited HDAC2/4-EphA2 axis in breast cancer. (a) Cells were treated with HDAC2 and EphA2 siRNAs, and then western blot analysis was performed to detect the level of indicated proteins. (b) Cells were treated with various concentrations of WW437; then qPCR was performed to detect the mRNA level of EphA2. (c) After treatment with WW437 for 24 h, western blot analysis was performed to detect Sp1 expression. (d) Cells were treated with HDAC2 and HDAC4 siRNAs, and then western blot analysis was performed to detect Sp1 expression. (e) Cells were treated with Sp1 siRNAs, and then western blot analysis was performed to detect EphA2 expression. (f) After treatment with WW437 for 24 h or Sp1 siRNAs for 48 h, ChIP assays were conducted to detect the binding capability of Sp1 to the promoter of EphA2. (g, h) MDA231 cells were treated with WW437 and nuclear extracts were prepared. The immunoprecipitation was performed using anti-HDAC2, anti-HDAC4 or Sp1 antibodies. The immunoprecipitated pellets were analysed by western blotting with indicated antibodies. (i) MDA231 cells were treated with WW437 for 24 h, ChIP-re-ChIP assays were conducted to detected the binding capability of HDAC2/Sp1 or HDAC4/Sp1 to the promoter of EphA2.