Fig. 1: Low transcription levels of MACROH2A2 contribute to GBM aggressiveness.
From: macroH2A2 antagonizes epigenetic programs of stemness in glioblastoma
a, b Kaplan–Meier survival analysis of a all high-grade gliomas in TCGA GBM cohort60 (n = 336) and b adult IDH-wildtype glioblastoma patients (GSE1601161; n = 86) based on MACROH2A2 (mH2A2) transcription levels. mH2A2-low and -high groups were determined by median gene expression. The shaded region represents a 95% confidence interval. P value was obtained by log-rank test. c Hazard ratios for macroH2A2 expression in GSE16011 (n = 155) in a multivariate Cox regression model adjusting for other factors relevant for glioblastoma (age, IDH mutation status). Error bars represent 95% confidence intervals. d Kaplan–Meier survival analysis of adult IDH-wildtype glioblastoma patients (n = 86) separated by transcriptional subtype (GSE16011). The shaded region represents a 95% confidence interval. P values obtained by log-rank test. e Kaplan–Meier survival analysis of adult IDH-wildtype primary glioblastoma patients with the proneural transcriptional subtype (GLASS consortium; n = 17). The shaded region represents a 95% confidence interval. P values obtained by log-rank test. f Expression of MACROH2A2 (mH2A2) in the scRNA-seq GBM dataset by ref. 8 plotted on a 2D state diagram. g CIBERSORTx decomposition of RNA-seq datasets from control and knockdown G523 cells (three biological replicates per condition); (p = 0.021 (NPC shScr vs shMH2A2a, p = 0.01823 (MES shScr vs shMH2A2a); NPC p = 0.0075 shScr vs shMH2A2b; MES p = 0.0116 shScr vs shMH2A2b) [p values: two-tailed unpaired T-test with Welch’s correction]. Error bars represent standard deviation. h Immunohistochemistry of macroH2A2 and macroH2A1 in a primary patient glioblastoma specimen (scale bar: 50 µ). The experiment was repeated on three independent primary clinical samples.
