Analysis of gene expression in TET1 depleted colorectal cancer Colo320DM cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE84396 | GEO | 2017/01/01
SECONDARY ACCESSION(S): PRJNA329081
REPOSITORIES: GEO
Similar Datasets
Project description:We aimed to analyze the relationship between TET1 and aberrant CpG methylation in colorectal cancer (CRC). We established three stable TET1 knockdown clones and negative control clones of Colo320DM cells, and carried out DNA methylation analysis with HumanMethylation450 BeadChip.
2017-01-01 | GSE84397 | GEO
Project description:We aimed to analyze the relationship between TET1 and aberrant CpG methylation in colorectal cancer (CRC). We established two stable TET1 knockdown clones and negative control clones of HCT116 cells, and carried out gene expression analysis with Agilent Human Gene Expression microarray kit.
2017-01-01 | GSE84398 | GEO
Project description:We aimed to analyze the relationship between TET1 and aberrant CpG methylation in colorectal cancer (CRC). We established two stable TET1 knockdown clones and negative control clones of HCT116 cells, and carried out DNA methylation analysis with HumanMethylation450 BeadChip.
2017-01-01 | GSE84399 | GEO
Project description:Transcriptional profiling of HCT116 cells transfected with either control siRNA or TET1 siRNA was analyzed using whole human genome microarrays. To identify genes regulated by TET1 in colorectal cancer, HCT116 cells were transfected with either control siRNA or TET1 siRNA, and total RNA was extracted from biologically duplicated samples.
2015-09-04 | E-GEOD-66512 | biostudies-arrayexpress
Project description:To establish a genomewide miRNA profile of colorectal cancer-derived induced pluripotent cancer cell lines (CRC-iPC). CRC-iPC clones and two parental cell lines were subjected to miRNA microarray analysis using SurePrint Human MiRNA Microarray Release 21.0 (Agilent). In order to identify the differentially-expressed miRNAs after OSKM-reprogramming, the miRNA expression of CRC-iPCs was relatively compared to that of parental colorectal cancer cell lines. Using a stringent selection criteria of log2(fold change) (FC) ≥ 2.0 or < -2.0 and p-value < 0.05, a total of 102 statistically significant differentially-expressed miRNAs were identified. Amongst the 102 miRNAs, 50 miRNAs were down-regulated and 52 miRNAs were up-regulated. Four miRNAs (miR-362-5p, miR-532-3p, miR-125b-5p, and miR199a-3p) were randomly selected for validation by quantitative real-time PCR, the results were consistent with that of the microarray results. To establish a genomewide miRNA profile of colorectal cancer-derived induced pluripotent cancer cell lines (CRC-iPC). CRC-iPC clones and two parental cell lines were subjected to miRNA microarray analysis using SurePrint Human MiRNA Microarray Release 21.0 (Agilent). In order to identify the differentially-expressed miRNAs after OSKM-reprogramming, the miRNA expression of CRC-iPCs was relatively compared to that of parental colorectal cancer cell lines. Using a stringent selection criteria of log2(fold change) (FC) ≥ 2.0 or < -2.0 and p-value < 0.05, a total of 102 statistically significant differentially-expressed miRNAs were identified. Amongst the 102 miRNAs, 50 miRNAs were down-regulated and 52 miRNAs were up-regulated. Four miRNAs (miR-362-5p, miR-532-3p, miR-125b-5p, and miR199a-3p) were randomly selected for validation by quantitative real-time PCR, the results were consistent with that of the microarray results.
2018-07-31 | GSE87280 | GEO
Project description:Colorectal cancer (CRC) ranks third for incidence and second for number of deaths among cancer types worldwide. Poor patient survival, due to inadequate response to currently available treatment regimens, points out to the urgent requirement for personalized therapy in CRC patients. Our aim was to provide mechanistic insights into the pro-tumorigenic role of the RNA-binding protein ESRP1, which is highly expressed in a subset of CRC patients. We show that, in CRC cells, ESRP1 binds to and has the same trend in expression as RAC1b, a well-known tumor promoter. Thus, RAC1b may be a potential therapeutic target in ESRP1-overexpressing CRC. RNA binding proteins are well recognized as critical regulators of tumorigenic processes through their capacity to modulate RNA biogenesis, including alternative splicing, RNA stability and mRNA translation. The RNA binding protein Epithelial Splicing Regulatory Protein 1 (ESRP1) can act as tumor suppressor or promoter in a cell type- and disease context-dependent manner. We have previously shown that elevated expression of ESRP1 in colorectal cancer cells can drive tumor progression. To gain further insights into the pro-tumorigenic mechanism of action of ESRP1, we performed cDNA microarray analysis on two colorectal cells lines modulated for ESRP1 expression. Intriguingly, RAC1b was highly expressed, both at mRNA and protein levels, in ESRP1-overexpressing cells, while the opposite trend was observed in ESRP1-silenced CRC cells. Moreover, RAC1 and RAC1b mRNA co-immunoprecipitate with ESRP1 protein. Silencing of RAC1b expression significantly reduced the number of soft agar colonies formed by ESRP1-overexpressing cells, suggesting that ESRP1 acted, at least partially, through RAC1b in its tumor-promoting activities in CRC cells. Thus, our data provide molecular cues on targetable candidates in CRC cases with high ESRP1 expression.
2021-08-31 | GSE180126 | GEO
Project description:To identify new markers for colorectal cancer we scrutinized the methylation status by methyl-CpG immunoprecipitation followed by global methylation profiling on a CpG island microarray, as altered expression could drive genomic and chromosomal instability observed in these tumors. We show for the first time hypermethylation of MMP9, DNMT3A, and LIG4 in CRC which was confirmed in two independent ethnic CRC patients groups. Hypermethylation of the LIG4 promoter is a new mechanism to control ligase IV expression. It may represent a new epigenetic marker for colorectal cancer independent of known markers. Methylation profiling in 16 tumors of colorectal cancer patients compared to matched normal tissue of these patients
2013-12-31 | E-GEOD-47413 | biostudies-arrayexpress
Project description:To identify novel hypermethylated genes in colorectal cancer (CRC) and to test their potential application in CRC early diagnosis, we performed a genome-wide screening of 57,723 CpG dinucleotides covering 4,010 genes in paired DNA samples extracted from 3 fresh frozen CRC tissues and their matching non-tumor adjacent tissues from a cohort of 3 CRC patients undergoing curative surgery using MIRA-based microarray. We also validated candidate hypermethylated genes screened by MIRA-based microarray in independent CRC samples using combined bisulfite restriction analysis. A total of 297 CpG dinucleotides in CRC covering 211 genes were found to be hypermethylated in CRC tissues. From these 211 candidate methylated genes, seven novel methylated genes were picked up for validation and three genes were confirmed to be methylated in cancer samples but not in non-cancer samples.We also compared the methylation levels of these three novel hypermethylated genes with those of Vimentin and SEPT9, well-known hypermethylated genes in CRC, and found that methylated PHOX2B, FGF12 and GAD2 were better than methylated Vimentin and SEPT9 in differentiating CRC cancer tissue from normal tissue. Significant enrichment analysis of GO terms of the hypermethylated genes showed that a high proportion of hypermethylated genes in tumor tissues are involved in regulation of transcription. Paired experiments, colorectal cancer tissue vs. adjacent non-cancer tissue. Biological replicates: 3 cancer replicates, 3 paired non-cancer replicates.
2011-11-14 | E-GEOD-33545 | biostudies-arrayexpress
Project description:Aberrant DNA methylation is frequently observed in colorectal cancer (CRC), but the underlying mechanisms and pathological consequences are poorly understood. Ten-Eleven Translocation (TET) dioxygenases and Thymine DNA Glycosylase (TDG) are involved in active DNA demethylation by generating and removing novel oxidized cytosine species. TET1 and TDG mutations, and alterations of the levels of oxidized cytosines have been identified in human CRC. To clarify the biological significance of the TET-TDG demethylation axis in intestinal tumorigenesis, we generated ApcMin mice that are devoid of Tet1 and/or Tdg, and characterized the methylome and transcriptome of intestinal adenomas by DREAM and RNA sequencing, respectively. Tet1-deficient and Tet1/Tdg-double heterozygous ApcMin adenomas manifested increased adenoma size and features of erosion or invasion, whereas an increased number (>30) of adenomas was found in Tdg-mutant ApcMin mice. Methylome analysis revealed progressive loss of global DNA hypomethylation in colonic adenomas from Tet1- and Tdg-deficient ApcMin mice, and hypermethylation of CpG islands in Tet1-deficient ApcMin mice. In addition, RNA sequencing showed upregulation of genes in inflammatory, immune and interferon response in Tet1- and Tdg-mutant colonic adenomas compared to control ApcMin adenomas. The corresponding 135-gene inflammatory signature separated human colonic adenocarcinomas into four groups, closely aligned with their microsatellite or chromosomal instability profile, and characterized by different levels of DNA methylation and DNMT1 expression levels that anti-correlated with TET1 expression levels. These findings demonstrate a novel mechanism of epigenetic regulation during intestinal tumorigenesis by which TET1-TDG-mediated active DNA demethylation decreases not only methylation levels, but also inflammatory/interferon/immune response, which impinges on the intrinsic features of genomic instability of the tumors. This study establishes a novel link, via inflammatory response, between epigenomic and genomic instability.
2023-10-01 | GSE179526 | GEO
Project description:TET1 oxidizes methylated cytosine into 5-hydroxymethylcytosine, resulting in regulation of DNA methylation and gene expression. Full length TET1 (TET1-FL) has a CXXC domain that binds to unmethylated stretches of CpG dinucleotides known as CpG islands (CGIs). This CXXC domain allows TET1 to protect CGIs from aberrant methylation but it also limits its ability to regulate genes outside of CGIs. Here we report a novel isoform of TET1 (TET1-ALT) that has a unique transcription start site from an alternate promoter in intron 2, yielding a protein with a unique translation start site. Importantly, TET1-ALT lacks the CXXC domain but retains the catalytic domain. To identify the gene expression targets of TET1-ALT and to compare them to the gene expression targets of TET1-FL, we performed RNA-seq on HEK293T cells that overexpress either Empty Vector (Control), TET1-FL or TET1-ALT.
2017-05-12 | GSE93619 | GEO