Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA144737 | ENA |
REPOSITORIES: ENA
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Project description:In our study we applied a genome-wide DNA methylation analysis approach, MethylCap-seq, to map the differentially methylated regions in 24 tumor and matched normal colon samples. In total, 2687 frequently hypermethylated and 468 frequently hypomethylated regions were identified, which include potential biomarkers for CRC diagnosis. Hypermethylation in the tumor samples was enriched at CpG islands and gene promoters, while hypomethylation was distributed throughout the genome. Using epigenetic data from human embryonic stem cells, we show that frequent differentially methylated regions (DMRs) coincide with bivalent loci in human embryonic stem cells. DNA methylation is commonly thought to lead to cancer gene related silencing, however integration of publically available expression analysis shows that 75% of the frequently hypermethylation genes were most likely already lowly or not expressed in normal tissue. Collectively, our study provides genome-wide DNA methylation maps of colon cancer, comprehensive lists of DMRs, and gives further clues on the role of aberrant DNA methylation in CRC formation. To investigate DNA methylation in CRC in a genome-wide unbiased fashion, we applied MethylCap-seq. This method involves capture of methylated DNA using the MBD domain of MeCP2, and subsequent next-generation Illumina sequencing of eluted DNA. In addition, we compared MethylCap with RNA-seq and ChIP-seq profiles of H3K4me3 and H3K27me3 for the colon cancer tumor cell line HCT116 (HCT116 WT) and the cell line of HCT116 with DNMT1 and DNMT3b knockout (HCT116 DKO).
2012-10-26 | E-GEOD-39068 | biostudies-arrayexpress
Project description:Genome-wide association studies (GWAS) have identified single nucleotide polymorphisms (SNPs) associated with increased risk for colorectal cancer (CRC). A molecular understanding of the functional consequences of this genetic variation is complicated because most GWAS SNPs are located in non-coding regions. After identifying H3K27Ac peaks in HCT116 colon cancer cells that harbor SNPs associated with an increased risk for CRC, we used CRISPR/Cas9 nuclease to delete 2 CRC risk-associated H3K27Ac peaks (E7 and E24), a peak that is not associated with CRC risk (18qE) and a region that doesn?t have H3K27Ac peak (18qNE) from HCT116 cells and analyzed effects on the transcriptome and epigenome. We also deleted E7 region from HEK 293 cells and analyzed effects on the transcriptome of HEK 293. We also confirmed the physical interaction between enhancers of our interest and their putative target genes. Analysis of RNA-seq data and ChIP-seq between control clones and enhancer deleted clones in HCT116 cell. For Control, gRNA empty vectorplasmid was transfected with Cas9-GFP. For Deletion, gRNAs that have enhancer target sequences were transfected along with Cas9-GFP. Cells with high GFP expression were identified using fluorescence-activated cell sorting. Sorted cells were plated into individual wells of a 24 well plate and then re-plated as single cells in 10cm dishes and subsequently expanded for further analyses. Samples used in this study were clonal populations. Interaction profiling of enhancers of interest with putative target genes using 4C-seq
2016-01-12 | E-GEOD-72631 | biostudies-arrayexpress
Project description:RNA-seq of HCT116 and HCT116-DKO colon cancer cell lines
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Project description:The obesity epidemic is associated with increased colorectal cancer (CRC) risk and progression, the mechanisms of which remain unclear. In obese individuals, hypertrophic epiploic adipose tissue (EPAT), attached to the colon, has unique characteristics compared to other fats. We hypothesized that this understudied fat could serve as a tumor-promoting tissue and developed a novel microphysiological system (MPS) for human EPAT-dependent colorectal cancer (CRC-MPS). In CRC-MPS, obese EPAT, unlike lean EPAT, considerably attracted colon cancer HT29-GFP cells and enhanced their growth. Conditioned media (CM) from the obese CRC-MPS significantly increased the growth and migration of HT29 and HCT116 cells (p< 0.001). In HT29 cells, CM stimulated differential gene expression (hOEC867) linked to cancer, tumor morphology, and metabolism similar to those in the colon of high-fat-diet obese mice. The hOEC867signature represented pathways found in human colon cancer. In unsupervised clustering, hOEC867separated transcriptomes of colon cancer samples from normal with high significance (PCA,p =9.6 × 10−11). These genes, validated in CM-treated HT29 cells (p< 0.05), regulate the cell cycle, cancer stem cells, methylation, and metastasis, and are similarly altered in human colon cancer (TCGA). These findings highlight a tumor-promoting role of EPAT in CRC facilitated with obesity and establishes a platform to explore critical mechanisms and develop effective treatments.
2023-05-04 | GSE228532 | GEO
Project description:Stable XIAP knockdown in HCT116 colon cancer cells
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Project description:Human colorectal cancer cell line CRC#21: ALDH-high cells vs. ALDH-low cells
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Project description:The transcriptome profiling of human colon cancer cell HCT116
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Project description:Induction of ER stress in HCT116 colon cancer cells
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Project description:To screen for epigenetically silenced miRNAs, wecarried out miRNA microarray analysis in three colorectal cancer (CRC) cell lines (HCT116, DLD-1 and RKO) treated with or without 5-aza-2'-deoxycytidine (aza). HCT116 and RKO cells were also treated with aza plus 4-phenylbutyric acid (PBA). In addition, we analyzed HCT116 cells in which the DNA methyltransferase genes DNMT1 and DNMT3B were genetically disrupted (double knockout; DKO cells), thereby abrogating DNA methylation. Expression of a majority of miRNAs was downregulated in all three CRC cell lines tested, as compared to normal colonic mucosa. DAC treatment upregulated expression of a large number of miRNAs in all three CRC cell lines, and combination treatment with DAC plus PBA induced even greater numbers of miRNAs in CRC cells. The most profound effect on the miRNA expression profile was induced by genetic disruption of DNMT1 and DNMT3B in HCT116 cells. CRC cells were treated with 5-aza-2’-deoxycytidine (aza) or aza plus 4-phenylbutyrate (PBA). Nomal colon RNA was purchased from BioChain. Expression of 470 miRNAs was analyzed using Human miRNA Microarray V1 (G4470A; Agilent technologies, Santa Clara, CA, USA).
2011-07-01 | E-GEOD-29900 | biostudies-arrayexpress