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P16 epimutation modulates the tumor microenvironment and promotes malignancy of Apc-mutant colon cancer

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

PROVIDER: PRJNA881366 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21610312_1.fastq.gz	Fastqsanger.gz
	SRR21610312_2.fastq.gz	Fastqsanger.gz
	SRR21610313_1.fastq.gz	Fastqsanger.gz
	SRR21610313_2.fastq.gz	Fastqsanger.gz
	SRR21610314_1.fastq.gz	Fastqsanger.gz

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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.

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

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

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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.

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

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