Homeobox genes gain trimethylation of histone H3 lysine 4 in glioblastoma tissue
العنوان: | Homeobox genes gain trimethylation of histone H3 lysine 4 in glioblastoma tissue |
---|---|
المؤلفون: | Kun Luo, Dong-Hui Luo, Hao Wen |
المصدر: | Bioscience Reports |
بيانات النشر: | Portland Press Ltd., 2016. |
سنة النشر: | 2016 |
مصطلحات موضوعية: | 0301 basic medicine, Chromatin Immunoprecipitation, Histone H3 Lysine 4, Biophysics, Biology, urologic and male genital diseases, Methylation, Biochemistry, glioblastoma multiforme (GBM), Epigenesis, Genetic, Histones, 03 medical and health sciences, Histone H3, Humans, Epigenetics, Promoter Regions, Genetic, Molecular Biology, Original Paper, Brain Neoplasms, urogenital system, Lysine, Genes, Homeobox, S13, H3K4me3, homeobox genes, Cell Biology, DNA Methylation, Middle Aged, Cadherins, Original Papers, S12, nervous system diseases, Chromatin, Gene Expression Regulation, Neoplastic, 030104 developmental biology, CpG site, S39, DNA methylation, Cancer research, Homeobox, Female, Glioblastoma |
الوصف: | We revealed that in GBM homeobox genes gain tri-methylation on lysine 4 of histone H3 (H3K4me3), whereas the cell–cell adhesion-related cadherin genes lose H3K4me3, suggesting that the H3K4me3 alteration is related to the formation and migration of GBM cells. 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). Tri-methylation on lysine 4 of histone H3 (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 in H3K4me3 in GBM, especially at promoters and CpG islands. In GBM, homeobox genes gain H3K4me3, whereas the cell–cell adhesion-related cadherin genes lose H3K4me3. The products of the homeobox genes are highly connected with Ras-signalling and PI3K-Akt signalling pathways. Using The Cancer Genome Atlas (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 epidermal growth factor receptor (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. |
تدمد: | 1573-4935 0144-8463 |
URL الوصول: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::044d2a501d75c906fb3a165cf29a2ff7 https://doi.org/10.1042/bsr20160028 |
حقوق: | OPEN |
رقم الأكسشن: | edsair.doi.dedup.....044d2a501d75c906fb3a165cf29a2ff7 |
قاعدة البيانات: | OpenAIRE |
تدمد: | 15734935 01448463 |
---|