CNV analysis of normal brain and glioma samples II
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PROVIDER: PRJNA676116 | ENA |
REPOSITORIES: ENA
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Project description:CNV analysis of normal brain and glioma samples
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Project description:In human, the 39 coding HOX genes and 18 referenced non-coding antisense transcripts are arranged in four genomic clusters named HOXA, B, C, and D. This highly conserved family belongs to the homeobox class of genes that encode transcription factors required for normal development. Therefore, HOX gene deregulation might contribute to the development of many cancer types. Here, we study HOX gene deregulation in adult glioma, a common type of primary brain tumor. We performed extensive molecular analysis of tumor samples, classified according to their isocitrate dehydrogenase (IDH1) gene mutation status, and of glioma stem cells. We found widespread expression of sense and antisense HOX transcripts only in aggressive (IDHwt) glioma samples, although the four HOX clusters displayed DNA hypermethylation. Integrative analysis of expression-, DNA methylation- and histone modification signatures along the clusters revealed that HOX gene upregulation relies on canonical and alternative bivalent CpG island promoters that escape hypermethylation. H3K27me3 loss at these promoters emerges as the main cause of widespread HOX gene upregulation in IDHwt glioma cell lines and tumors. Our study provides the first comprehensive description of the epigenetic changes at HOX clusters and their contribution to the transcriptional changes observed in adult glioma. It also identified putative "master" HOX proteins that might contribute to the tumorigenic potential of glioma stem cells.
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Project description:Aberrant DNA methylation is a well-defined feature of cancer cells that is commonly associated to transcriptional alteration. Nonetheless, a primary role of this defect in genome-wide cancer-associated gene misregulation is still being questioned. Here, we used adult glioma, a widespread type of brain tumor, to evaluate the relative contribution of DNA methylation-dependent and -independent mechanisms on transcriptional alteration at CpG-island/promoter-associated genes in cancer cells. By extensive molecular analyses conducted in both IDH wild-type (IDHwt) and IDH mutated (IDHmut) samples, we show that DNA hypermethylation affects only a minority of genes that show a loss or a gain of expression. In IDHwt samples, for instance, more than 75% of aberrantly repressed genes do not display DNA methylation defect at their CpG-island promoter. Rather, an alteration in the H3K27me3 signature is the predominant molecular defect at misregulated genes. We also observed that a bivalent chromatin signature in stem cell might not only predispose genes to hypermethylation, as widely documented, but more generally to all type of transcriptional alterations. In addition, we evidenced that transcriptional strength in healthy brain influences the choice between DNA methylation- or H3K27me3- associated silencing pathway at repressed genes in glioma. Combined our study supports a model whereby the altered developmental control of H3K27me3 dynamics, and more specifically defects in the interplay between polycomb protein complexes and brain-specific transcriptional machinery, is the main cause of transcriptional alteration in glioma cells. Together our study provides a comprehensive and revisited picture of epigenetic gene deregulations in cancer. Our observations are also of importance for the design of drugs that aims to target cancer epigenetic defects.
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Project description:A human microarray comprising 1658 human genome probes was used to evaluate the specific expression of miRNA between brian glioma stem cells (GSC) and normal neural stem cells(NSC). 2 total RNA samples are analyzed, brian glioma stem cells (GSC) and normal neural stem cells(NSC). cell type: brain glioma stem cells:GSC_1, GSC_2, GSC_3 ; cell line: normal neural stem cells: NSC_1, NSC_2, NSC_3 biological replicate: NSC_1, NSC_2, NSC_3; biological replicate: GSC_1, GSC_2, GSC_3
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Project description:A human cDNA microarray comprising 29,187 human genome probes was used to evaluate the transcriptional changes between brian glioma stem cells (GSC) and normal neural stem cells(NSC). There were 6 samples that were analyzed, 3 samples were from glioma stem cells and the other 3 samples form normal neural stem cells were controls. cell type: brain glioma stem cells:GSC_H004, GSC_H005, GSC_H006 ; cell line: normal neural stem cells: NSC_H001, NSC_H002, NSC_H003 biological replicate: NSC_H001, NSC_H002, NSC_H003; biological replicate: GSC_H004, GSC_H005, GSC_H006
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Project description:Aberrant DNA methylation is a well-defined feature of cancer cells that is commonly associated to transcriptional alteration. Nonetheless, a primary role of this defect in genome-wide cancer-associated gene misregulation is still being questioned. Here, we used adult glioma, a widespread type of brain tumor, to evaluate the relative contribution of DNA methylation-dependent and -independent mechanisms on transcriptional alteration at CpG-island/promoter-associated genes in cancer cells. By extensive molecular analyses conducted in both IDH wild-type (IDHwt) and IDH mutated (IDHmut) samples, we show that DNA hypermethylation affects only a minority of genes that show a loss or a gain of expression. In IDHwt samples, for instance, more than 75% of aberrantly repressed genes do not display DNA methylation defect at their CpG-island promoter. Rather, an alteration in the H3K27me3 signature is the predominant molecular defect at misregulated genes. We also observed that a bivalent chromatin signature in stem cell might not only predispose genes to hypermethylation, as widely documented, but more generally to all type of transcriptional alterations. In addition, we evidenced that transcriptional strength in healthy brain influences the choice between DNA methylation- or H3K27me3- associated silencing pathway at repressed genes in glioma. Combined our study supports a model whereby the altered developmental control of H3K27me3 dynamics, and more specifically defects in the interplay between polycomb protein complexes and brain-specific transcriptional machinery, is the main cause of transcriptional alteration in glioma cells. Together our study provides a comprehensive and revisited picture of epigenetic gene deregulations in cancer. Our observations are also of importance for the design of drugs that aims to target cancer epigenetic defects.
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