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. 2015 Mar 19;17(11):1463–1473. doi: 10.1093/neuonc/nov041

Fig. 4.

Fig. 4.

HDAC and KDM1A inhibition alter TAp73 expression. LN-18 cells transfected with control or KDM1A shRNA were treated with 5 µM vorinostat for 24 hours: (A) TA, Δexon 2 (Δex2), Δexon 2 and 3 (Δex2/3), ΔN or ΔN′ isoforms of p73 were measured by RT-qPCR., or (B) p73 protein expression was evaluated by Western blot. (C) LN-18 cells were treated with 5 µM vorinostat, 1 mM tranylcypromine, or the combination and TAp73 mRNA expression was evaluated by qPCR. (D) LN-18 cells were treated with 5 µM vorinostat, and TAp73 mRNA expression was measured at the indicated time points. (E) TAp73 expression was measured in p53-null glioblastoma cells (LNZ308) were transfected with vector or Flag-tagged wild-type p53 followed by treatment with 5 µM vorinostat, 1 mM tranylcypromine, or the combination. (F) Viability was measured in wild-type (p73+/+), p73-deficient (p73−/−), or ΔN-p73-deficient (ΔN−/−) mouse embryonic fibroblasts treated with 5 µM vorinostat, 1 mM tranylcypromine, or the combination for 24 hours. n = 3, mean ± SEM. *P ≤ .05, **P ≤ .01, ***P ≤ .001.