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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

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2011-07-01 | E-GEOD-29900 | biostudies-arrayexpress

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

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

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2016-05-31 | GSE79041 | GEO

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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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