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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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(CTA) expression after exposure to 5-aza-2'-deoxycytidine in HCT116 cells

ABSTRACT: The expression of CTAs is normally restricted to gametogenic tissue but is often reactivated in the tumorigenic setting. This tumorigenic reactivation is thought to be due to global demethylation events during tumorigenesis. To test this, we employed an affymetrix microarray in the hypermethylated colorectal carcinoma tumor-derived cell line, HCT116, following 5-aza-2'-deoxycytidine treatment. We used microarray analysis to uncover genes whose expression is modulated by DNA methylation in the colorectal carcinoma tumor derived cell line, HCT116. HCT116 cells were exposed to 5-aza-2'-deoxycytidine for 72 hours. Total RNA was isolated and hybridized on to Affymetrix microarrays.

ORGANISM(S): Homo sapiens

SUBMITTER: Min Soo Kim

PROVIDER: E-GEOD-79041 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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microRNA expression signatures in colorectal cancer cell lines with demethylating treatment

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

Genes regulated by miR-34b/c and DAC

Project description:We found frequent epigenetic silencing of microRNA-34b/c in human colorectal cancer. Introduction of miR-34b/c into a colorectal cancer cell line induced significant changes in gene expression profile. We also found overlap between the genes downregulated by miR-34b/c and those downregulated by DAC. Keywords: dose response A colorecal cancer cell line HCT116 was transfected with miR-34b or -c precursor or negative control. Also, HCT116 was treated with 5-aza-2'-deoxycytidine (DAC) or mock. Genes up- or downregulated by miR-34b/c and those by DAC was compared.

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Project description:We used bs-ATLAS-seq to comprehensively map the genomic location and assess the DNA methylation status of human full-length LINE-1 elements (L1). The approach is focused on the youngest family (L1HS), but it also catches a significant fraction of L1PA2 to L1PA8 elements. This was performed in HCT116 cells treated by the DNA methyltransferase inhibitor 5-aza-2’-deoxycytidine (5-aza) or in mock-treated cells (DMSO).

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Project description:Promoter methylation is able to induce downregulation of gene expression. 5-Aza-2'-deoxycytidine(Aza), methytransferase inhibitor, induce CpG demethylation. Here, 5-Aza-2'-deoxycytidine(Aza) is treated in a human breast cancer cell, MCF7, for detection of gene expression change. To analyze gene expression change by aza, control RNA isolated from MCF-7 was compared with RNA isolated from MCF-7 treated with 5uM and 10uM aza.

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Analysis of Promoter Methylation in Breast Cancer

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2011-03-07 | E-GEOD-26990 | biostudies-arrayexpress

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Project description:Initial screening for potential metastases suppressors down regulated by methylation was performed using lung cancer cell line models specific for site-specific metastasation. Gene expression profiling and qRT-PCR validations were conducted on tumor tissues from primary lung cancer (LC) and brain metastasis. HERC5 was further characterized for the methylation pattern. Three human lung cancer cell lines H1993, H1395 and were compared to the (SV40)-transformed human bronchial epithelial cell line BEAS-2B in order to find genes, which might be specifically involved in brain metastasis formation. The cell lines were treated with 5-Aza-2'-deoxycytidine in order to find genes potentially down regulated by methylation. The non-tumorigenic cell line BEAS-2B was used to control for stress response after the treatment with 5-Aza-2'-deoxycytidine.

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(CTA) expression after exposure to 5-aza-2'-deoxycytidine in HCT116 cells

Project description:The expression of CTAs is normally restricted to gametogenic tissue but is often reactivated in the tumorigenic setting. This tumorigenic reactivation is thought to be due to global demethylation events during tumorigenesis. To test this, we employed an affymetrix microarray in the hypermethylated colorectal carcinoma tumor-derived cell line, HCT116, following 5-aza-2'-deoxycytidine treatment. We used microarray analysis to uncover genes whose expression is modulated by DNA methylation in the colorectal carcinoma tumor derived cell line, HCT116.

2016-05-31 | GSE79041 | GEO

MicroRNA profiling of HCT-116 versus HCT-116 treated with 5-aza-2'-deoxycytidine processing human colon cancer cell lines

Project description:UCRs expression signature of HCT-116 cell lines versus HCT-116 cell line treated with DNA methylation inhibitor 5-aza-2'-deoxycytidine

2010-03-09 | E-MTAB-196 | biostudies-arrayexpress

Acute hypersensitivity of pluripotent testicular cancer-derived embryonal carcinoma to low-dose 5-aza deoxycytidine (part 1)

Project description:Human embryonal carcinoma (EC) cells are the stem cells of nonseminoma testicular germ cells tumors (TGCTs) and share remarkable similarities to human embryonic stem (ES) cells. In prior work we found that EC cells are hypersensitive to low nanomolar doses of 5-aza deoxycytidine (5-aza) and that this hypersensitivity partially depended on unusually high levels of the DNA methyltransferase, DNMT3B. We show here that low-dose 5-aza treatment results in DNA damage and induction of p53 in NT2/D1 cells. In addition, low-dose 5-aza results in global and gene specific promoter DNA hypomethylation. Low-dose 5-aza induces a p53 transcriptional signature distinct from that induced with cisplatin in NT2/D1 cells and also uniquely downregulates genes associated with pluripotency including NANOG, SOX2, GDF3 and Myc target genes. Changes in the p53 and pluripotency signatures with 5-aza were to a large extent dependent on high levels of DNMT3B. In contrast to the majority of p53 target genes upregulated by 5-aza that did not show DNA hypomethylation, several other genes induced with 5-aza had corresponding decreases in promoter methylation. These genes include RIN1, SOX15, GPER, and TLR4 and are novel candidate tumors suppressors in TGCTs. Our studies suggest that the hypersensitivity of NT2/D1 cells to low-dose 5-aza is multifactorial and involves the combined activation of p53 targets, repression of pluripotency genes, and activation of genes repressed by DNA methylation. Low-dose 5-aza therapy may be a general strategy to treat those tumors that are sustained by cells with embryonic stem-like properties. Total RNA obtained from NT2/D1-R1 sh control or NT2/D1-R1 sh DNMT3B knockdown cells treated with vehicle or 10 nM 5-aza deoxycytidine for 3 days. Four groups in biological triplicate for total of 12 hybridizations on Illumina HT-12v3 beadarray.

2012-12-01 | E-GEOD-42644 | biostudies-arrayexpress

Acute hypersensitivity of pluripotent testicular cancer-derived embryonal carcinoma to low-dose 5-aza deoxycytidine (part 3)

Project description:Human embryonal carcinoma (EC) cells are the stem cells of nonseminoma testicular germ cells tumors (TGCTs) and share remarkable similarities to human embryonic stem (ES) cells. In prior work we found that EC cells are hypersensitive to low nanomolar doses of 5-aza deoxycytidine (5-aza) and that this hypersensitivity partially depended on unusually high levels of the DNA methyltransferase, DNMT3B. We show here that low-dose 5-aza treatment results in DNA damage and induction of p53 in NT2/D1 cells. In addition, low-dose 5-aza results in global and gene specific promoter DNA hypomethylation. Low-dose 5-aza induces a p53 transcriptional signature distinct from that induced with cisplatin in NT2/D1 cells and also uniquely downregulates genes associated with pluripotency including NANOG, SOX2, GDF3 and Myc target genes. Changes in the p53 and pluripotency signatures with 5-aza were to a large extent dependent on high levels of DNMT3B. In contrast to the majority of p53 target genes upregulated by 5-aza that did not show DNA hypomethylation, several other genes induced with 5-aza had corresponding decreases in promoter methylation. These genes include RIN1, SOX15, GPER, and TLR4 and are novel candidate tumors suppressors in TGCTs. Our studies suggest that the hypersensitivity of NT2/D1 cells to low-dose 5-aza is multifactorial and involves the combined activation of p53 targets, repression of pluripotency genes, and activation of genes repressed by DNA methylation. Low-dose 5-aza therapy may be a general strategy to treat those tumors that are sustained by cells with embryonic stem-like properties. Genomic DNA obtained from NT2/D1-R1 sh control or NT2/D1-R1 sh DNMT3B knockdown cells treated with vehicle or 10 nM 5-aza deoxycytidine for 3 days. Four groups in biological triplicate for total of 12 hybridizations on Illumina HumanMethylation27 BeadChip.

2012-12-01 | E-GEOD-42646 | biostudies-arrayexpress

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