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Fig. 4 | Clinical Epigenetics

Fig. 4

From: KAT3B-p300 and H3AcK18/H3AcK14 levels are prognostic markers for kidney ccRCC tumor aggressiveness and target of KAT inhibitor CPTH2

Fig. 4

Treatment with CPTH2 and p300si in ccRCC 786-O cells show similar effects. a Western blot analysis of bulk histone preparations extracted from 786-O cells at increasing times of CPTH2 (100 μM) treatment sequentially hybridized with anti-AcH3, anti-H3AcK18, and anti-GAPDH as internal standard. b The same experiment performed in 786-O treated for p300si at increasing times in comparison with untreated nc. c Immunohistochemical staining of selective histone H3AcK14 and H3AcK18 in 786-O cells untreated, in DMSO and treated with CPTH2 (100 μM) for 48 h. d The same analysis performed in 786-O cells after 48 h p300si and nc control, hybridized with anti-p300, anti H3AcK14, and anti H3AcK18. e Histograms show the level of AcH3, H3AcK14, and H3AcK18 normalized to unmodified UMH3 found in 786-O cells treated with 24 and 48 h with CPTH2 (100 μM) and p300 inhibitor C646 (10 μM). f Comparison of mRNA levels of tumor markers AKT1 (green), TGFb-2 (red), and HIF-1α (blue) carried out by RT-qPCR in cells treated at increased indicated times for p300si (heavy colors) and with CPTH2, (100 μM), (light colors)

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