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Dietary folate and cofactors accelerate age-dependent p16 epimutation to promote intestinal tumorigenesis

ABSTRACT: Dietary folate and cofactors accelerate age-dependent p16 epimutation to promote intestinal tumorigenesis

PROVIDER: PRJNA1019771 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26139300_1.fastq.gz	Fastqsanger.gz
	SRR26139300_2.fastq.gz	Fastqsanger.gz
	SRR26139301_1.fastq.gz	Fastqsanger.gz
	SRR26139301_2.fastq.gz	Fastqsanger.gz
	SRR26139302_1.fastq.gz	Fastqsanger.gz

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Dietary folate and cofactors accelerate age-dependent p16 epimutation to promote intestinal tumorigenesis

Project description:We use a mouse model of age-dependent p16 epimutation, in which the p16 gene activity is directly controlled by promoter DNA methylation. We show p16 epimutation is modulated by folate and cofactors in dietary supplementation, which leads to increased colon cancer risk. Importantly, our findings provide functional evidence concerning the safety of folate fortification in the general population.

2024-08-19 | GSE243762 | GEO

Dietary Folate and Cofactors Accelerate Age-dependent p16 Epimutation to Promote Intestinal Tumorigenesis.

Project description:The extent to which non-genetic environmental factors, such as diet, contribute to carcinogenesis has been long debated. One potential mechanism for the effects of environmental factors is through epigenetic modifications that affect gene expression without changing the underlying DNA sequence. However, the functional cooperation between dietary factors and cancer-causing epigenetic regulation is largely unknown. Here, we use a mouse model of age-dependent p16 epimutation, in which the p16 gene activity is directly controlled by promoter DNA methylation. We show p16 epimutation is modulated by folate and cofactors in dietary supplementation, which leads to increased colon cancer risk. Importantly, our findings provide functional evidence concerning the safety of folate fortification in the general population.SignificanceOur study demonstrates that dietary folate and cofactors modulate tumor-suppressor gene methylation to increase intestinal tumorigenesis. Our findings highlight the need for monitoring the long-term safety of folate fortification in high-risk individuals.

| S-EPMC10798135 | biostudies-literature

p16 epimutation modulates the tumor microenvironment and promotes malignancy of Apc-mutant colon cancer (RNA-Seq)

Project description:Using a mouse model of engineered p16 promoter hypermethylation (p16cis/cis), we found that p16 epimutation cooperates with mutant Apc to promote colon cancer development. Therefore, we performed RNA-seq analysis to identify genes regulated by p16 epimutation that contribute to intestinal carcinogenesis.

2023-08-02 | GSE213566 | GEO

p16 epimutation modulates the tumor microenvironment and promotes malignancy of Apc-mutant colon cancer (scRNA-Seq)

Project description:Methylation of p16 promoter resulting in epigenetic gene silencing- known as p16 epimutation- is common in human colorectal cancer (CRC). Using mouse models, we demonstrated that p16 epimutation cooperates with mutant Apc to promote colon cancer development. To comprehensively characterize immune function within the tumor microenvironment (TME), we performed single-cell RNA sequencing (scRNA-seq) of colon tumors in these animals.

2023-08-02 | GSE213567 | GEO

p16 epimutation modulates the tumor microenvironment and promotes malignancy of Apc-mutant colon cancer

Project description:We previously generated a mouse model of p16 epimutation (named as p16cis/cis) through targeted knock-in of a 140-bp Alu-related DNA sequence (cis-element) that facilitates the spread of DNA methylation at promoter CpG islands (CGIs) in cis (Yu et al. JCI, 2014). We generated primary mouse embryonic fibroblasts (MEFs) from p16cis/cis and control mice. By whole genome bisulfite sequencing (WGBS) for comprehensive DNA methylation profiling, we showed that cis-element-mediated approach specifically induces p16 promoter hypermethylation.

2023-08-02 | GSE214032 | GEO

p16 epimutation modulates the tumor microenvironment and promotes malignancy of Apc-mutant colon cancer

Project description:p16 epimutation modulates the tumor microenvironment and promotes malignancy of Apc-mutant colon cancer

| PRJNA883661 | ENA

p16 epimutation modulates the tumor microenvironment and promotes malignancy of Apc-mutant colon cancer

Project description:p16 epimutation modulates the tumor microenvironment and promotes malignancy of Apc-mutant colon cancer

| PRJNA881366 | ENA

p16 epimutation modulates the tumor microenvironment and promotes malignancy of Apc-mutant colon cancer (scRNA-Seq)

Project description:p16 epimutation modulates the tumor microenvironment and promotes malignancy of Apc-mutant colon cancer (scRNA-Seq)

| PRJNA881381 | ENA

p16 epimutation modulates the tumor microenvironment and promotes malignancy of Apc-mutant colon cancer (RNA-Seq)

Project description:p16 epimutation modulates the tumor microenvironment and promotes malignancy of Apc-mutant colon cancer (RNA-Seq)

| PRJNA881378 | ENA

Molecular properties of epimutation hotspots

Project description:Mistakes in the maintenance of CG methylation is a source of heritable epimutations in plants. Multigenerational surveys indicate that the rate of these stochastic events varies substantially across the genome, with some regions harboring localized “epimutation hotspots”. Using Arabidopsis as a model, we show that epimutation hotspots are indexed by a specific set of chromatin states (CS) that map to sub-regions of gene body methylation genes. Although these regions comprise only ~12% of all CGs in the genome, they account for ~63% of all epimutation events per unit time. Molecular profiling revealed that these regions contain unique sequence features, harbor steady-state intermediate methylation levels, and act as putative targets of antagonistic DNA methylation pathways. We further demonstrate that experimentally-induced shifts in steady-state methylation in these hotspot regions are sufficient to significantly alter local epimutation intensities. Our work thus lays foundation for dissecting the molecular mechanisms of epimutation hotspots in plants.

2021-12-02 | GSE178684 | GEO

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