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DNA methylation analysis of Colon Cancer cell line SW48

ABSTRACT: We combined gene expression experiments in response to HDAC inhibitor Depsipeptide with DNA methylation level to assess gene reactivation arising from hypermethylated promoters.

ORGANISM(S): Homo sapiens

PROVIDER: GSE34427 | GEO | 2012/04/04

SECONDARY ACCESSION(S): PRJNA156387

REPOSITORIES: GEO

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DNA methylation analysis of Colon Cancer cell line SW48

Project description:We combined gene expression experiments in response to HDAC inhibitor Depsipeptide with DNA methylation level to assess gene reactivation arising from hypermethylated promoters. We did one experiment with 1 untreated and 1 treated batch of cells

2012-04-03 | E-GEOD-34427 | biostudies-arrayexpress

Colon Cancer cell line YB5 untreated cells vs YB5 treated 24h with Depsipeptide at 20 nM

Project description:Study the effect of HDACi Depsipeptide on gene expression. We combined these data with whole genome DNA methylation microarray to test the reactivation of genes that have an hypermethylated promoter region.

2012-04-04 | GSE34077 | GEO

Colon Cancer cell line YB5 untreated cells vs YB5 treated 24h with Depsipeptide at 20 nM

2012-04-03 | E-GEOD-34077 | biostudies-arrayexpress

Rpd3L HDAC links H3K4me3 to transcriptional repression memory

Project description:Transcriptional memory is critical for the faster reactivation of necessary genes upon environmental changes and requires that the genes were previously in an active state. However, whether transcriptional repression also displays “memory” of the prior transcriptionally inactive state remains unknown. In this study, we show that transcriptional repression of approximately 540 genes in yeast occurs much more rapidly if the genes have been previously repressed during carbon source shifts. This novel transcriptional response has been termed transcriptional repression memory(TREM). Interestingly, Rpd3L histone deacetylase (HDAC), targeted to active promoters induces TREM. Mutants for Rpd3L exhibit increased acetylation at active promoters and delay TREM and RNA PolII dissociation significantly. Surprisingly, the interaction between H3K4me3 and Rpd3L via the Pho23 PHD finger is sufficient to induce histone deacetylation and TREM by Rpd3L. Therefore, we propose that an active mark, H3K4me3 enriched at promoters, instructs Rpd3L HDAC to induce histone deacetylation and TREM.

2018-10-23 | E-MTAB-6551 | biostudies-arrayexpress

Expression and DNA methylation of colon cancer cell lines

Project description:This SuperSeries is composed of the following subset Series: GSE34077: Colon Cancer cell line YB5 untreated cells vs YB5 treated 24h with Depsipeptide at 20 nM GSE34427: DNA methylation analysis of Colon Cancer cell line SW48 Refer to individual Series

2012-04-03 | E-GEOD-34429 | biostudies-arrayexpress

Digital Restriction Enzyme Analysis of Methylation (DREAM) of SW48 colon cancer cell line genomic DNA.

2015-09-08 | GSE66296 | GEO

Transcription profiling of human HDAC-42 SEG-1 esophageal adenocarcinoma cells

Project description:The role of acid and bile salts in the pathogenesis of esophageal carcinoma arising from Barrett's metaplasia has been well established. Cell proliferation of Barrett's epithelium in response to pulsatile acid exposure has since been confirmed in vivo using endoscopy specimens. Histone deactylases (HDACs) modulate nucleosomal packaging of DNA, thereby influencing gene transcription and multiple cancer-associated processes. Thus, we conducted microarray analysis to assess the ability of HDAC-42 to modulate key acid-induced changes as well as to impact other genes altered as the normal esophageal epithelium progresses along the metaplasia-dysplasia-esophageal adenocarcinoma continuum. Experiment Overall Design: SEG-1 cells were pretreated for 24 hours with vehicle or HDAC-42, pulsed with media or acidified media (pH 3.5; 20 mins at 37C), replenished with media or HDAC-42, and harvested 6 hours later. Global gene expression analysis was conducted using the human genome chip U133 2.0 Plus.

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The Effects of NDRG2 Overexpression on Cell Proliferation and Invasiveness of SW48 Colorectal Cancer Cell Line.

Project description:BACKGROUND:Colorectal cancer (CRC) is one of the most common causes of cancer-related death in the world. The expression of N-myc downstream-regulated gene 2 (NDRG2) is down-regulated in CRC. The aim of this study was to investigate the effect of NDRG2 overexpression on cell proliferation and invasive potential of SW48 cells. METHODS:SW48 cells were transfected with a plasmid overexpressing NDRG2. After stable transfection, the effect of NDRG2 overexpression on cell proliferation was evaluated by MTT assay. The effects of NDRG2 overexpression on cell migration, invasion and cell motility and matrix metalloproteinase 9 (MMP9) activities were also investigated using matrigel transwell assay, wound healing assay and gelatin zymography, respectively. RESULTS:MTT assay showed that overexpression of NDRG2 caused attenuation of SW48 cell proliferation. Transwell and wound healing assay revealed that NDRG2 overexpression led to inhibition of migration, invasion, and motility of SW48 cells. The overexpression of NDRG2 also reduced the activity of secreted MMP-9. CONCLUSIONS:The results of this study suggest that NDRG2 overexpression inhibits proliferation and invasive potential of SW48 cells, which likely occurs via suppression of MMP-9 activity.

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HDAC-42 modulates acid-induced gene expression in human SEG-1 esophageal adenocarcinoma cells

Project description:The role of acid and bile salts in the pathogenesis of esophageal carcinoma arising from Barrett's metaplasia has been well established. Cell proliferation of Barrett's epithelium in response to pulsatile acid exposure has since been confirmed in vivo using endoscopy specimens. Histone deactylases (HDACs) modulate nucleosomal packaging of DNA, thereby influencing gene transcription and multiple cancer-associated processes. Thus, we conducted microarray analysis to assess the ability of HDAC-42 to modulate key acid-induced changes as well as to impact other genes altered as the normal esophageal epithelium progresses along the metaplasia-dysplasia-esophageal adenocarcinoma continuum. Keywords: acid-pulsed cells pretreated with HDAC inhibitor or vehicle

2007-07-30 | GSE7964 | GEO

Digital Restriction Enzyme Analysis of Methylation (DREAM) of SW48 colon cancer cell line genomic DNA.

Project description:We analyzed levels of 5-methyl cytosine nnnn CCCGGG target sites by sequential restriction digest by SmaI and XmaI enzymes, ligating Illumina adaptors to the restriction fragments and reading methylation-specific signatures at the ends of restriction fragments by paired ends Illumina high throughput sequencing. Digital restriction enzyme analysis of methylation (DREAM) was performed to determine the methylation profile of SW48 colon cancer cell line genomic DNA. Genomic DNA spiked in with unmethylated, partially methylated and fully methylated standards was sequentially cut at CCCGGG sites with the methylation-sensitive enzyme SmaI (blunt ends) and its methylation-tolerant neoschizomer XmaI (5'CCGG overhangs), creating different end sequences that represented methylation status of the CCCGGG sites. These end sequences were analyzed by Illumina high throughput sequencing. Methylation status at individual CCCGGG sites across the genome was determined by counting the methylated reads with the CCGGG signature and unmethylated reads with the GGG signature at the beginnings of the sequencing reads after alignment to the human genome.

2015-09-08 | E-GEOD-66296 | biostudies-arrayexpress

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