Fig. 6

MYC represses autophagy. a ChIP-seq analysis for Myc binding to the promoters of Vps18, Map1lc3b, Atg4d, and Gaparapl2 performed in mouse group 3 medulloblastoma tumorspheres overexpressing Myc, MB (Trp53^−/− overexpressing Myc) (n = 3 independent experiments). b ChIP analyses of the MAP1LC3B promoter using anti-MYC antibody performed in HeLa cells treated with SAHA (20 μM for 24 h) or DMSO (n = 3 biologically independent samples). c RT-qPCR of autophagy genes in tumorspheres Trp53^−/− overexpressing Myc (MB), (n = 10 biologically independent samples). d Comparative LC3 immunoblots of tumorspheres Trp53^−/− overexpressing Myc and control Trp53^−/− cells. e Quantification of the LC3II/LC3I ratio normalized to Coomassie stained immunoblots, used as loading control. C = Control (Trp53^−/−) cells (n = 3 biologically independent samples); G3 = tumorspheres Trp53^−/− overexpressing Myc (n = 15 biologically independent samples). f Expression levels of several autophagic genes in U2OS cells with silenced MYC expression. g RT-qPCR of GABARAPL2, MAP1LC3B, PIK3C3 and SQSTM1 was performed in HeLa cells silenced for MYC (shMYC) (n = 3 biologically independent samples) and treated with SAHA (8 μM for 24 h). Boxes represent the mean value and bar inside the box represents median value; upper bar represents maximum of distribution; lower bar represents minimum of distribution (95% confidence level). Graphs are presented as mean ± SD. Statistical analysis was performed using the Student t-test. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001