Figure 4.
In vitro treatment with the histone deactylase inhibitor trichostatin A (TSA) causes euchromatinization of the RRP22 promoter in the glioblastoma cell lines U87MG and A172. Quantitative real‐time PCR analysis of RRP22 promoter DNA binding to anti‐H3ac and anti‐H4ac after euchromatinizing treatment with TSA. (A) Note that in the glioblastoma cell line, A172 the TSA (red) curve for anti‐H3ac‐bound RRP22 is shifted to the left relative to the CTRL (blue) curve, while the reference curves (input) for TSA and CTRL pass the threshold (Ct) at an approximately equal cycle number. This corresponds to markedly increased RRP22 promoter DNA levels bound to H3ac after treatment with TSA. Abscissa, cycle number; ordinate, relative amount of PCR product. (B) After TSA treatment, an increase of promoter DNA binding of RRP22 to H3ac (left) and H4ac (right) is observed in both cell lines (ratio TSA/CTRL >1). p21, positive control gene (CDKN1A/p21WAF1) known to be inactivated by histone modifications in gliomas; GAPDH, negative control gene not regulated by histone modifications.