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Loss of hydroxymethylcytosine is an independent adverse prognostic factor in clear cell Renal Cell Carcinoma (ccRCC) and can be abrogated by ascorbic acid mediated TET activation

ABSTRACT: Loss of hydroxymethylcytosine is an independent adverse prognostic factor in clear cell Renal Cell Carcinoma (ccRCC) and can be abrogated by ascorbic acid mediated TET activation

PROVIDER: PRJNA512847 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8392770.fastq.gz	Fastqsanger.gz
	SRR8392771.fastq.gz	Fastqsanger.gz
	SRR8392772.fastq.gz	Fastqsanger.gz
	SRR8392773.fastq.gz	Fastqsanger.gz
	SRR8392766.fastq.gz	Fastqsanger.gz

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Similar Datasets

Loss of hydroxymethylcytosine is an independent adverse prognostic factor in clear cell Renal Cell Carcinoma (ccRCC) and can be abrogated by ascorbic acid mediated TET activation

Project description:The experiment was performed to study high resolution gene specific changes induced by Ascorbic acid tretament in clear cell RCC cells (786-0 cell line)

2019-04-03 | GSE124610 | GEO

Ascorbic acid–induced TET activation mitigates adverse hydroxymethylcystosine loss in renal cell carcinoma

Project description:Although clear cell renal cell carcinoma (ccRCC) has been shown to result in widespread aberrant cytosine methylation and loss of 5-hydroxymethylcytosine (5hmC), the prognostic impact and therapeutic targeting of tis epigenetic aberrancy has not been fully explored. Analysis of 576 primary ccRCC samples demonstrated that loss of 5hmC was significantly associated with aggressive clinicopathologic features and was an independent adverse prognostic factor. Loss of 5hmC alsopredicted reduced progression-free survival after resection of nonmetastatic disease. The loss of 5hmC in ccRCC was not due to mutational or transcriptional inactivation of ten eleven translocation (TET) (4. AUTHOR: TET also appears as Tet. If these mean the same thing, choose one style to use throughout.) enzymes, but to their functional inactivation by l -2-hydroxyglutarate (L2HG), which was overexpressed due to the deletion and underexpression of L2HG dehydrogenase(L2HGDH). Ascorbic acid (AA) reduced methylation and restored genome-wide 5hmC levels via TET activation. Fluorescence quenching of the recombinant TET-2 protein was unaffected by L2HG in the presence of AA. Pharmacologic AA treatment led to reduced growth of ccRCC in vitro and reduced tumor growth in vivo, with increased intratumoral 5hmC. These data demonstrate that reduced 5hmC is associated with reduced survival in ccRCC and provide a preclinical rationale for exploring the therapeutic potential of high-dose AA in ccRCC.

2019-04-03 | GSE126823 | GEO

Ascorbic acid-induced TET activation mitigates adverse hydroxymethylcytosine loss in renal cell carcinoma.

Project description:Although clear cell renal cell carcinoma (ccRCC) has been shown to result in widespread aberrant cytosine methylation and loss of 5-hydroxymethylcytosine (5hmC), the prognostic impact and therapeutic targeting of this epigenetic aberrancy has not been fully explored. Analysis of 576 primary ccRCC samples demonstrated that loss of 5hmC was strongly associated with aggressive clinicopathologic features and was an independent adverse prognostic factor. Loss of 5hmC also predicted reduced progression-free survival after resection of nonmetastatic disease. The loss of 5hmC in ccRCC was not due to mutational or transcriptional inactivation of ten eleven translocation (TET) enzymes, but to their functional inactivation by l-2-hydroxyglutarate (L2HG), which was overexpressed due to the deletion and underexpression of L2HG dehydrogenase (L2HGDH). Ascorbic acid (AA) reduced methylation and restored genome-wide 5hmC levels via TET activation. Fluorescence quenching of the recombinant TET-2 protein was unaffected by L2HG in the presence of AA. Pharmacologic AA treatment led to reduced growth of ccRCC in vitro and reduced tumor growth in vivo, with increased intratumoral 5hmC. These data demonstrate that reduced 5hmC is associated with reduced survival in ccRCC and provide a preclinical rationale for exploring the therapeutic potential of high-dose AA in ccRCC.

| S-EPMC6436862 | biostudies-literature

Ascorbic acid–induced TET activation mitigates adverse hydroxymethylcystosine loss in renal cell carcinoma

Project description:Ascorbic acid–induced TET activation mitigates adverse hydroxymethylcystosine loss in renal cell carcinoma

| PRJNA523404 | ENA

TET-catalyzed 5-hydroxymethylcytosine regulates gene expression in differentiating colonocytes and colon cancer

Project description:5-hydroxymethylcytosine (5-mC) and gene expression profiling of T84 cell differentiation; 5-hmC profiling of colon cancer colonocyte fractions

2015-12-09 | GSE69333 | GEO

Expression data from ccRCC specimens

Project description:To identify a therapeutic candidate target molecule for ccRCC, we analyzed the microRNA (miRNA) expression signatures in ccRCC clinical specimens. 9 matched pair (normal tissue and ccRCC tissue) plus 7 ccRCC tissue were analyzed for miRNA-microarray

2014-02-20 | E-GEOD-55138 | biostudies-arrayexpress

Tet-assisted bisulfite sequencing of 5-hydroxymethylcytosine.

Project description:A complete understanding of the potential function of 5-hydroxymethylcytosine (5-hmC), a DNA cytosine modification in mammalian cells, requires an accurate single-base resolution sequencing method. Here we describe a modified bisulfite-sequencing method, Tet-assisted bisulfite sequencing (TAB-seq), which can identify 5-hmC at single-base resolution, as well as determine its abundance at each modification site. This protocol involves ?-glucosyltransferase (?-GT)-mediated protection of 5-hmC (glucosylation) and recombinant mouse Tet1(mTet1)-mediated oxidation of 5-methylcytosine (5-mC) to 5-carboxylcytosine (5-caC). After the subsequent bisulfite treatment and PCR amplification, both cytosine and 5-caC (derived from 5-mC) are converted to thymine (T), whereas 5-hmC reads as C. The treated genomic DNA is suitable for both whole-genome and locus-specific sequencing. The entire procedure (which does not include data analysis) can be completed in 14 d for whole-genome sequencing or 7 d for locus-specific sequencing.

| S-EPMC3641661 | biostudies-literature

TET-catalyzed 5-hydroxymethylcytosine regulates gene expression in differentiating colonocytes and colon cancer

Project description:5-hydroxymethylcytosine (5-mC) and gene expression profiling of T84 cell differentiation; 5-hmC profiling of colon cancer colonocyte fractions T84 cell differentiation was monitored as cells formed confluent monolayers in tissue culture

2015-12-09 | E-GEOD-69333 | biostudies-arrayexpress

Ascorbic acid enhances Tet-mediated 5-methylcytosine oxidation and promotes DNA demethylation in mammals.

Project description:DNA demethylation occurs in multiple cellular processes but its regulation is poorly understood. Here we report that a vital nutrient factor ascorbic acid (AA), or vitamin C (Vc), induces DNA demethylation in mammalian cells. The levels of active 5mC oxidation products, 5-formylcytosine and 5-carboxylcytosine, increase by more than one magnitude of order in mouse ES cells when cultured in the presence of AA. In cells deleted of Tet1 and Tet2 dioxygenase genes, AA does not facilitate 5mC oxidation. The AA effect is however restored when Tet2 was re-expressed in the mutant cells. The enhancing effect of AA on 5mC oxidation and DNA demethylation was also observed in a mouse model deficient in AA synthesis. Our results thus reveal a role of AA in the regulation of DNA modification, which might mediate a plethora of functions of AA.

2015-01-01 | GSE43262 | GEO

Tet-mediated formation of 5-hydroxymethylcytosine in RNA.

Project description:Oxidation of 5-methylcytosine in DNA by ten-eleven translocation (Tet) family of enzymes has been demonstrated to play a significant role in epigenetic regulation in mammals. We found that Tet enzymes also possess the activity of catalyzing the formation of 5-hydroxymethylcytidine (5-hmrC) in RNA in vitro. In addition, the catalytic domains of all three Tet enzymes as well as full-length Tet3 could induce the formation of 5-hmrC in human cells. Moreover, 5-hmrC was present at appreciable levels (∼1 per 5000 5-methylcytidine) in RNA of mammalian cells and tissues. Our results suggest the involvement of this oxidation in RNA biology.

| S-EPMC4140497 | biostudies-literature

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