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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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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

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Clear cell renal cell carcinoma (ccRCC) samples

Project description:To select signatures of ccRCC, 265 ccRCC samples were obtained from the Van Andel Research Institute. Gene expression profiles of 265 samples were determined using the HG-U133_Plus_2 platform.

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MBOAT7 loss of function in clear cell Renal Carcinoma (ccRCC)

Project description:We demonstrated an increase in MBOAT7 and downstream phosphatidylinositol products in ccRCC. This RNAseq was of two loss of function clones and wild-type in the Caki-1 cell model (ccRCC cell line).

2020-02-26 | GSE131881 | GEO

LncRNA from metastatic clear cell renal cell carcinoma (ccRCC) compared with non-metastatic clear cell renal carcinoma

Project description:A total of 3 metastatic and 3 non-metastatic ccRCC tissues were collected from patients. These tissues were flash frozen in liquid nitrogen immediately after surgery and subsequently stored at -80℃. All the resected nodules or metastatic masses were identified as renal tumor by pathologic examination. No patients received anticancer treatments before surgery in this study. We analyzed gene expression microarray data from our gene chip with 3 metastatic ccRCC tissues compared with 3 non-metastatic ccRCC tissues.

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Expression data for HIF1alpha-regulated genes in clear cell renal carcinoma cells (ccRCC)

Project description:Gene expression profiling was performed in ccRCC cells, which either express both HIF1alpha and HIF2alpha (either naturally or by virtue of induced expression of HIF1alpha) or express HIF2alpha alone (either naturally or by virtue of a HIF1alpha shRNA), to identify genes regulated by HIF1alpha in ccRCC cells.

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Epigenome analysis of clear cell renal cell carcinoma (ccRCC) tissue versus matched normal kidney tissue

Project description:Genome wide DNA methylation profiling of clear cell renal cell carcinoma (ccRCC) tissue versus matched normal kidney tissue. TheÂ IlluminaÂ Infinium 450k Human DNA methylation Beadchip was used to obtain DNA methylation profiles across approximatelyÂ 450,000 CpGs in tumor and adjacent normal kidney tissue samples from ccRCC patients. Samples included 46 paired fresh frozen ccRCC tumor and adjacent normal kidney tissues. Bisulphite converted DNA from the 92 samples were hybridised to the Illumina Infinium 450 Human Methylation Beadchip v1.2

2015-10-26 | E-GEOD-61441 | biostudies-arrayexpress

Epigenome analysis of clear cell renal cell carcinoma (ccRCC) tissue versus matched normal kidney tissue

Project description:Genome wide DNA methylation profiling of clear cell renal cell carcinoma (ccRCC) tissue versus matched normal kidney tissue. The Illumina Infinium 450k Human DNA methylation Beadchip was used to obtain DNA methylation profiles across approximately 450,000 CpGs in tumor and adjacent normal kidney tissue samples from ccRCC patients. Samples included 46 paired fresh frozen ccRCC tumor and adjacent normal kidney tissues.

2015-10-26 | GSE61441 | GEO

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