RNA-seq of HCT116 and HCT116-DKO colon cancer cell lines
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE82338 | GEO | 2019/06/07
REPOSITORIES: GEO
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Project description:Genome-wide view of the interplay between methylation and RNA expression in this colorectal cancer model was obtained. RNA-sequencing of HCT116 cell line, the DNMT1 and DNMT3B double knock-out HCT116 cell line (DKO), and 7 additional colorectal cell lines.
2013-10-01 | E-GEOD-45332 | biostudies-arrayexpress
Project description:This study aimed to investigate the link between DNA methylation and protein expression on a genome wide level, using a combination of MBD-sequencing and shotgun and positional proteomics on two human colon cancer cell lines: a wild type HCT116 cell line and a double knock out HCT116 cell line (DNMT1 -/- and DNMT3b -/-). The protein content of the HCT116 WT and DKO cell lines was not only analyzed using a standard shotgun proteomics approach, but also with the N-terminal COFRADIC technique (Staes et al., 2011), in order to determine the (alternative) translation start site of the expressed proteins.
2015-08-19 | PXD000304 | Pride
Project description:CpG island promoter hypermethylation of tumor suppressor genes is a common hallmark of human cancer, and new large-scale epigenomic technologies might be useful in our attempts to define the complete DNA hypermethylome of tumor cells. Here we report a functional search for hypermethylated CpG islands using the colorectal cancer cell line HCT-116, in which two major DNA methyltransferases, DNMT1 and DNMT3b, have been genetically disrupted (DKOcells). Using methylated DNA immunoprecipitation (MeDIP) methodology in conjunction with promoter microarray analyses we found that DKO cells experience a significant loss of hypermethylated CpG islands. Further characterization of these candidate sequences demonstrates CpG island promoter hypermethylation and silencing of genes with potentially important roles in tumorigenesis, such as the Ras guanine-nucleotide release factor RASGRF2, the apoptosis-associated basic helixloop transcription factor BHLHB9, and the homeobox gene HOXD1. Hypermethylation of these genes occurs already in premalignant lesions and accumulates during tumorigenesis. Thus, our results demonstrate the usefulness of DNMT genetic disruption strategies combined with MeDIP in searching for unknown hypermethylated candidate genes in human cancer that might aid our understanding of the biology of the disease and be of potential translational use. Keywords: Human Proximal Promoter Array; DNA Methylation Comparative experiment: methylated DNA immunoprecipitated/INPUT(Total Genomic DNA) from the colon cancer cell line HCT116 wild type vs methylated DNA imonoprecipitated/INPUT from the colon cancer cell line HCT116 DNMT1/3b doubleknockout (DKO)
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Project description:We compare histone modifications, chromatin accessibility, and replication timing domain genome-wide in HCT116 colon cancer cells with its genetic derivative DKO cells which lack DNMT3B and DNMT1 activity and the fibrosarcoma cell line HT1080.
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2017-05-17 | GSE98990 | GEO
Project description:Genome wide DNA methylation profiling of colon adenocarcinoma cell line HCT116 wild type and with a genetic disruption of DNMT3B and DNMT1 (DKO). The Illumina Infinium 27k Human DNA methylation Beadchip v1.2 was used to obtain DNA methylation profiles across approximately 27,000 CpGs. For this study, we used two DKO subclones, DKO8 and DKO1, which retain approximately 45% and 5% of the HCT116 wild type global DNA methylation levels, respectively
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Project description:This is one of expressional parts of the study. These data were correlated to epigenetic changes and CG density of genes in analyzed cells. The whole study has a following summary: To elucidate possible roles of DNA methylation and chromatin marks in transcription, we performed epigenetic profiling of chromosome 19 in human bronchial epithelial cells (HBEC) and in the colorectal cancer cell line HCT116 as well as its counterpart with double knockout of DNMT1 and DNMT3B (HCT116-DKO). We found that H3K9me3 forms intragenic chromatin blocks along genes with low CpG density in the gene body. Analysis of H3K36me3 profiles indicated that this mark associates either with active genes with low CpG density and H3K9me3 in the gene body or with active genes with high CpG density and DNA hypermethylation in the gene body. In HCT116 cells with double knockout of DNMT1 and DNMT3B, transcription of genes with low CpG density in the gene body was highly elevated and associated with promoter DNA demethylation and rearrangement of H3K9me3 and H3K36me3 occupation. Our finding suggests that similar to DNA methylation, H3K9me3 may play a role in intragenic gene regulation. Further, we observed that a combination of low CpG density in gene bodies together with H3K9me3 and H3K36me3 marking is a specific epigenetic feature of zinc finger (ZNF) genes, which comprise 90% of all genes carrying both histone marks on chromosome 19. For high CpG density genes, transcription and H3K36me3 occupancy were not changed in condition of partial or intensive loss of DNA methylation in gene bodies in the HCT116-DKO cell line. siRNA experiments with SETD2 knockdown in both HBEC and HCT116-DKO cell lines failed to reduce DNA methylation in gene bodies under conditions of H3K36me3 depletion. Our study suggests that the H3K36me3 and DNA methylation marks in gene bodies are established independently from each other and points to similar functional roles of intragenic DNA methylation and intragenic H3K9me3 for CpG-rich and CpG-poor genes, respectively. To elucidate how a loss of DNA methylation affects a gene expression and epigenome we studied colon cancer cell line HCT116 and its derivative, HCT116 DNMT1-/- DNMT3b -/- (HCT116-DKO). According to previous studies HCT116-DKO is characterized by 95% of loss of DNA methylation. In HCT116 and HCT116-DKO cells, we profiled diverse epigenetic marks and gene expression. Further a crosstalk between epigenetic changes and transcriptional changes was analyzed. This is the expressional part of study.
2011-03-31 | E-GEOD-26018 | biostudies-arrayexpress
Project description:Genome wide DNA methylation profiling of colon adenocarcinoma cell line HCT116 wild type and with a genetic disruption of DNMT3B and DNMT1 (DKO). The Illumina Infinium 27k Human DNA methylation Beadchip v1.2 was used to obtain DNA methylation profiles across approximately 27,000 CpGs. For this study, we used two DKO subclones, DKO8 and DKO1, which retain approximately 45% and 5% of the HCT116 wild type global DNA methylation levels, respectively Bisulphite converted DNA from the 3 samples were hybridised to the Illumina Infinium 27k Human Methylation Beadchip v1.2
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Project description:DNA methylation is a key epigenetic modification involved in regulating gene expression and maintaining genomic integrity. Somatic patterns of DNA methylation are largely static, apart from focal dynamics at gene regulatory elements. To further advance our understanding of the role of DNA methylation in human development and disease, we inactivated all three catalytically active DNA methyltransferases in human embryonic stem cells (ESCs) using CRISPR/Cas9 genome editing. Disruption of DNMT3A or DNMT3B individually, as well as of both enzymes in tandem, creates viable, pluripotent cell lines with distinct effects on their DNA methylation landscape as assessed by whole-genome bisulfite sequencing. Surprisingly, in contrast to mouse, deletion of DNMT1 resulted in rapid cell death in human ESCs. To overcome the immediate lethality, we generated a doxycycline (DOX) responsive tTA-DNMT1* rescue line and readily obtained homozygous DNMT1 mutant lines. However, DOX-mediated repression of the exogenous DNMT1* initiates rapid, global loss of DNA methylation, followed by extensive cell death, demonstrating that DNA methylation is essential for human ESCs cultured in standard conditions. In summary, our data provide a comprehensive characterization of DNMT mutant ESCs, including single base genome-wide maps of their targets. RRBS methylation profiling of DNMT3A/3B DKO human ES cells
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Project description:This data includes regulatory factor profiling using DNase and ChIP-seq and methylation profiling using bisulfite-seq. We investigated CTCF occupancy in the context of reduced methylation by performing genome-wide profiling with chromatin immunoprecipitation (ChIP-seq) in HCT116 cells and DNMT1 and DNMT3B double knockout (DKO) HCT116 cells. We also profiled HCT116 and DKO using DNaseI-seq and ChIP-seq for trimethylation of histone 3 lysine 4 (H3K4me3) and acetylation of histone 3 lysine 27 (H3K27ac), Finally, we performed ChIP-seq on 3 replicates of mock-treated and 2 replicates of 5-aza-CdR-treated K562 cells.
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