Skip to main content
. Author manuscript; available in PMC: 2014 Oct 1.
Published in final edited form as: Mol Cancer Ther. 2013 Aug 12;12(10):10.1158/1535-7163.MCT-12-1242. doi: 10.1158/1535-7163.MCT-12-1242

Figure 4. HDAC1/2 regulate ATM expression.

Figure 4

(A.) After pre-treatment with the HDAC inhibitors vorinostat (1 μM), valproic acid (1 mM), or entinostat (1 μM), cells were treated with epirubicin (Epi.) and analyzed by western blot for activation and stabilization of p53. (B.) Cells nucleofected with siRNA pools targeting HDAC1, HDAC2, both HDAC1/2 or control scrambled sequences for 48 hours were examined by qRT-PCR for gene mRNA expression normalized to h.Gus examining HDAC (B.) and DNA repair genes (*p<0.05 vs. scramble) (D.). Western blot of HDACs, ATM, and acetylated tubulin expression from cells in (B). Cells transfected as in (B.) were treated with vehicle or 0.5 μM epirubicin (8 hours) and examined for activation of ATM and CHK2 by western blot (E.) and p53 response genes induction by qRT-PCR (*p<0.05 vs. epirubicin treated) (F.). (G.) Cell death was assayed by trypan blue inclusion in cells with depleted HDAC expression and treated with epirubicin. (*p<0.05 vs. epirubicin treated)