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Altered Ten Eleven Translocation Methylcytosine Dioxygenase Expression and DNA Hydroxymethylation in a Mouse Model of Prostate Cancer [RNA-seq]

ABSTRACT: Altered Ten Eleven Translocation Methylcytosine Dioxygenase Expression and DNA Hydroxymethylation in a Mouse Model of Prostate Cancer [RNA-seq]

PROVIDER: PRJNA1170308 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30913479_1.fastq.gz	Fastqsanger.gz
	SRR30913479_2.fastq.gz	Fastqsanger.gz
	SRR30913480_1.fastq.gz	Fastqsanger.gz
	SRR30913480_2.fastq.gz	Fastqsanger.gz
	SRR30913481_1.fastq.gz	Fastqsanger.gz

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Altered Ten Eleven Translocation Methylcytosine Dioxygenase Expression and DNA Hydroxymethylation in a Mouse Model of Prostate Cancer [hMeDIP-seq]

Project description:Altered Ten Eleven Translocation Methylcytosine Dioxygenase Expression and DNA Hydroxymethylation in a Mouse Model of Prostate Cancer [hMeDIP-seq]

| PRJNA1170307 | ENA

Altered Ten Eleven Translocation Methylcytosine Dioxygenase Expression and DNA Hydroxymethylation in a Mouse Model of Prostate Cancer [RNA-seq]

Project description:Background: DNA hydroxymethylation (5hmC) is known to be altered in human prostate cancer. An animal model is required to study the functional roles of the Ten Eleven Translocation (TET) DNA dioxygenases and the 5hmC modification in prostate cancer development and progression. Methods: We characterized Tet expression, global genomic 5hmC, and genome-wide 5hmC patterns, and the transcriptome, in the Transgenic Adenocarcinoma of Mouse Prostate (TRAMP) autochthonous model of prostate cancer. Results: We observed increased mRNA and protein expression of Tet1 in TRAMP samples, as compared to normal mouse prostate. Additionally, we found minimal expression of Tet2 mRNA overall, and Tet3 mRNA levels appeared similar in both sample types. However, TRAMP tumors expressed what appeared to be the inactive form of Tet3, versus the active form expressed in normal prostates. TRAMP tumors displayed global genomic hypohydroxymethylation (i.e., loss of 5hmC), and genome-wide analysis revealed widespread hypohydroxymethylation was interspersed with regions of locus specific hyperhydroxymethylation (i.e., increased 5hmC). The differentially hydroxymethylated regions correlated with altered gene expression, and pathway analyses indicated that these genes often participate in oncogenic pathways.Conclusions: Tet expression and 5hmC patterns are altered in the TRAMP model and closely match what has been observed in human prostate cancer, suggesting that TRAMP is a suitable model to study the role of Tets and 5hmC in prostate cancer development and progression.

2025-03-21 | GSE279077 | GEO

Altered Ten Eleven Translocation Methylcytosine Dioxygenase Expression and DNA Hydroxymethylation in a Mouse Model of Prostate Cancer [hMeDIP-seq]

2025-03-21 | GSE279076 | GEO

Ten-eleven translocation (Tet) methylcytosine dioxygenases dependent viral DNA demethylation mediates in vivo hepatitis B virus (HBV) biosynthesis

Project description:Liver-specific ten-eleven translocation methylcytosine dioxygenases 2 and 3 (Tet2 plus Tet3)-deficient hepatitis B virus (HBV) transgenic mice fail to support viral biosynthesis. The levels of viral transcription and replication intermediates are dramatically reduced. Hepatitis B core antigen (HBcAg) is only observed in a very limited number of pericentral hepatocytes in a pattern that is similar to glutamate-ammonia ligase (Glul), a -catenin target gene. HBV transcript abundance in Tet-deficient mice resembles that observed in wild-type neonatal mice. Furthermore, the RNA levels of several -catenin target genes including Glul, Lhpp, Notun, Oat, Slc1a2 and Tbx3, in Tet-deficient mice was also similar to that observed in wild-type neonatal mice. As HBV transcription is regulated by -catenin, these finding support the suggestion that neonatal Tet-deficiency might limit -catenin target gene expression, limiting viral biosynthesis. Additionally, HBV transgene DNA displays increased 5-methylcytosine (5mC) frequency at CpG sequences consistent with neonatal Tet-deficiency being responsible for decreased developmental viral DNA demethylation mediated by 5mC oxidation to 5-hydroxymethylcytosine (5hmC), a process that might be responsible for the reduction in cellular -catenin target gene expression and viral transcription and replication.

2023-11-29 | GSE242448 | GEO

Ten-eleven translocation (Tet) methylcytosine dioxygenases dependent viral DNA demethylation mediates in vivo hepatitis B virus (HBV) biosynthesis

Project description:Ten-eleven translocation (Tet) methylcytosine dioxygenases dependent viral DNA demethylation mediates in vivo hepatitis B virus (HBV) biosynthesis

| PRJNA1013490 | ENA

TET1 reprograms the epithelial ovarian cancer epigenome and reveals casein kinase 2α as a therapeutic target

Project description:Ten-eleven translocation methylcytosine dioxygenase-1, TET1, takes part in active DNA demethylation. This study showed that TET1 expression reprogramed ovarian cancer epigenome and correlated with poor survival in advanced-stage epithelial ovarian carcinoma (EOC).

2024-03-31 | GSE128098 | GEO

Association between ten-eleven methylcytosine dioxygenase 2 genetic variation and viral load in people with HIV.

Project description:IntroductionIdentifying genetic factors that influence HIV-pathogenesis is critical for understanding disease pathways. Previous studies have suggested a role for the human gene ten-eleven methylcytosine dioxygenase 2 (TET2) in modulating HIV-pathogenesis.MethodsWe assessed whether genetic variation in TET2 was associated with markers of HIV-pathogenesis using both gene level and single nucleotide polymorphism (SNP) level association in 8512 HIV-positive persons across five clinical trial cohorts.ResultsVariation at both the gene and SNP-level of TET2 was found to be associated with levels of HIV viral load (HIV-VL) consistently in the two cohorts that recruited antiretroviral-naïve participants. The SNPs occurred in two clusters of high linkage disequilibrium (LD), one associated with high HIV-VL and the other low HIV-VL, and were predominantly found in Black participants.ConclusionGenetic variation in TET2 was associated with HIV-VL in two large antiretroviral therapy (ART)-naive clinical trial cohorts. The role of TET2 in HIV-pathogenesis warrants further investigation.

| S-EPMC9894145 | biostudies-literature

An auto-suppression mechanism for Tet dioxygenase protects the mouse genome from oxidative demethylation

Project description:Dynamic DNA methylation and demethylation regulate gene expression during development. While DNA methyltransferases (DNMTs) establish and maintain cytosine methylation patterns, Ten-eleven translocation (Tet) dioxygenases catalyze sequential oxidation of 5-methylcytosine (5mC) to promote demethylation. Target-specific 5mC oxidation requires precise regulation of the Tet enzymatic activity. However, the mechanism underlying their activity control remains largely unexplored. Here we show a large low-complexity domain (LCD), present within the catalytic domain of Tet3, functions to repress the dioxygenase activity. Recombinant LCD-deleted Tet3 exhibits enhanced activity to convert 5mC into oxidized species. Deletion of the Tet3 LCD in mouse oocytes renders 5mC oxidation indiscriminately across the genome, leading to most prominently the derepression of ERVK retrotransposons and upregulation of adjacent genes. The extensive 5mC oxidation is associated with impairments in oocyte development. These findings suggest an intrinsic auto-regulatory mechanism of Tet3 dioxygenase operating to ensure a tight regulation of its enzymatic activity to achieve spatiotemporal specificity of methylome reprogramming during oocyte development.

2023-06-26 | GSE222618 | GEO

Genes regulated by both of Ten-Eleven translocation 3 and Tumor necrosis factor α in Rheumatoid arthritis fibroblast-like synoviocytes

Project description:As DNA demethylation is a dynamic epigenetic regulation in pattern formation of DNA methylation, we reasoned that DNA demethylation facilitates Rheumatoid arthritis (RA) progression. To address this point, we picked up the DNA dioxygenase family members (Ten-Eleven translocation: TET1/2/3) as these enzymes conduct the prime process of DNA demethylaion. Tumor necrosis factor α (TNFα) , one of the pro-inflammatory cytokines, was found effective in up-regulation in TET3 level in the cultured fibroblast-like synoviocytes (FLS), and the stimulated FLS cells exhibited high cell mobility with gene induction of cell-migration related factors in a TET3-dependent manner. From our findings, we presume that DNA demethylation mediated TET3 facilitates RA progression and chronicity as an epigenetic regulation.

2021-02-09 | GSE166389 | GEO

A low-complexity domain of Tet3 dioxygenase shields the oocyte methylome from oxidative erosion [RNA-seq]

2023-08-24 | GSE222500 | GEO