Glioblastoma multiforme (GBM) exhibits considerable heterogeneity and associates with genome-wide alterations of the repressed chromatin marks DNA methylation and H3 lysine 27 trimethylation (H3K27me3). H3K4me3 is an activating epigenetic mark that is enriched at promoter and promotes expression. It will be helpful in GBM diagnosis and treatment to identify the alteration of H3K4me3 between human GBM and GBM-surrounding tissues. Here, we performed an analysis using next-generation sequencing techniques to identify H3K4me3 modification in a case of GBM and the GBM-surrounding tissues. The results revealed a global decrease of H3K4me3 in GBM, especially at promoters and CpG islands. In GBM, homeobox genes gain H3K4me3; while the cell-cell adhesion-related cadherin genes lose H3K4me3. The products of the homeobox genes are highly connected with Ras-signaling and PI3K-Akt signaling pathways. Using TCGA data, we inferred the homeobox-regulated genes' expression is higher in 548 GBM cases than in 27 lower grade glioma cases giving that OLIG2 expression can be a reference. The results suggested that the H3K4me3 alteration is related to the formation and migration of GBM cells. We also found an extremely high reads count at EGFR promoter, probably due to an amplification of copy number. Our analysis provides a case study about the change of H3K4me3 during shift to GBM.
- Glioblastoma multiforme (GBM)
- Homeobox genes
- ©2016 The Author(s)
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