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Ribonucleotide excision repair is essential to prevent skin cancer

ABSTRACT: Ribonucleotide excision repair is essential to prevent skin cancer

PROVIDER: PRJNA473504 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7228800.fastq.gz	Fastqsanger.gz
	SRR7228810.fastq.gz	Fastqsanger.gz
	SRR7228820.fastq.gz	Fastqsanger.gz
	SRR7228830.fastq.gz	Fastqsanger.gz
	SRR7228840.fastq.gz	Fastqsanger.gz

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Ribonucleotide excision repair is essential to prevent skin cancer [CD49f+ epidermal cells]

Project description:Ribonucleotide excision repair is essential to prevent skin cancer [CD49f+ epidermal cells]

| PRJNA473507 | ENA

Ribonucleotide excision repair is essential to prevent skin cancer [CD45+ CD49f- epidermal cells]

Project description:Ribonucleotide excision repair is essential to prevent skin cancer [CD45+ CD49f- epidermal cells]

| PRJNA473510 | ENA

Ribonucleotide excision repair is essential to prevent skin cancer [CD49f+ epidermal cells]

Project description:Large numbers of ribonucleotides are incorporated into the eukaryotic nuclear genome during S-phase due to imperfect discrimination against ribonucleoside triphosphates by the replicative DNA polymerases. Ribonucleotides, by far the most common DNA lesion in replicating cells, destabilize the DNA, and an evolutionarily conserved DNA repair machinery, ribonucleotide excision repair (RER), ensures ribonucleotide removal. Complete lack of RER is embryonically lethal. Partial loss-of-function mutations in the genes encoding subunits of RNase H2, the enzyme essential for initiation of RER, cause the SLE-related type I interferonopathy Aicardi-Goutières syndrome. Here we establish that selective inactivation of RER in mouse epidermis results in spontaneous DNA damage, epidermal hyperproliferation associated with loss of hair follicle stem cells and hair follicle function. The animals develop keratinocyte intraepithelial neoplasia and invasive squamous cell carcinoma with complete penetrance, despite potent type I interferon production and skin inflammation. Compromised RER-mediated genome maintenance might represent an important tumor-promoting principle in human cancer.

2019-05-29 | GSE115003 | GEO

Ribonucleotide excision repair is essential to prevent skin cancer [CD45+ CD49f- epidermal cells]

2019-05-29 | GSE115004 | GEO

Ribonucleotide excision repair prevents intestinal tumorigenesis

Project description:Ribonucleotide excision repair prevents intestinal tumorigenesis

| PRJNA436583 | ENA

Ribonucleotide excision repair prevents intestinal tumorigenesis

Project description:Insufficient repair of DNA lesions results in the acquisition of somatic mutations and displays the driving force in cancerogenesis. Ribonucleotide incorporation by eukaryotic DNA polymerases occurs during every round of genome duplication and represents by far the most frequent type of naturally occurring DNA lesions. RNAse H2 removes misincorporated ribonucleotides from genomic DNA in a process termed ribonucleotide excision repair (RER). Whether intestinal epithelial proliferation requires RER and whether abrogation of RER is involved in the etiology of cancerogenesis at all is unknown. Mice with an epithelial specific deletion of RNase H2 subunit b (H2bΔIEC) and co-deletion of the tumor suppressor p53 (H2b/p53ΔIEC) were generated and phenotyped at young and old age. RNA sequencing was performed in isolated epithelial cells and intestinal organoids. Mutational signature of spontaneous tumors from H2b/p53ΔIEC mice were characterized using exome sequencing. Association of tumor RNase H2 expression and patient survival was assessed in transcriptome data from 467 CRC patients. H2bΔIEC mice display chronic epithelial DNA damage and develop a p53-dependent proliferative exhaustion of the intestinal stem cell compartment. H2b/p53ΔIEC mice have restored epithelial proliferation and spontaneously develop small intestinal carcinomas. Resulting tumors display a distinct mutational signature characterized by T>G base substitutions at GpTpG trinucleotides. Transcriptome data from human colorectal cancer patients indicate that reduced RNase H2 expression is associated with poor survival in CRC. Conclusion: We propose a hitherto unappreciated role for RNase H2 as a tumor suppressor gene in CRC. Our mouse model provides a novel tool to study the impact of abrogated RER on intestinal carcinogenesis.

2018-10-01 | GSE111318 | GEO

Ribonucleotide excision repair is essential to prevent skin cancer

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-05-29 | GSE115005 | GEO

Ribonucleotide Excision Repair Is Essential to Prevent Squamous Cell Carcinoma of the Skin.

Project description:Because of imperfect discrimination against ribonucleoside triphosphates by the replicative DNA polymerases, large numbers of ribonucleotides are incorporated into the eukaryotic nuclear genome during S-phase. Ribonucleotides, by far the most common DNA lesion in replicating cells, destabilize the DNA, and an evolutionarily conserved DNA repair machinery, ribonucleotide excision repair (RER), ensures ribonucleotide removal. Whereas complete lack of RER is embryonically lethal, partial loss-of-function mutations in the genes encoding subunits of RNase H2, the enzyme essential for initiation of RER, cause the SLE-related type I interferonopathy Aicardi-Goutières syndrome. Here, we demonstrate that selective inactivation of RER in mouse epidermis results in spontaneous DNA damage and epidermal hyperproliferation associated with loss of hair follicle stem cells and hair follicle function. The animals developed keratinocyte intraepithelial neoplasia and invasive squamous cell carcinoma with complete penetrance, despite potent type I interferon production and skin inflammation. These results suggest that compromises to RER-mediated genome maintenance might represent an important tumor-promoting principle in human cancer.Significance: Selective inactivation of ribonucleotide excision repair by loss of RNase H2 in the murine epidermis results in spontaneous DNA damage, type I interferon response, skin inflammation, and development of squamous cell carcinoma. Cancer Res; 78(20); 5917-26. ©2018 AACR.

| S-EPMC6526525 | biostudies-literature

Genome-wide repair maps of nucleotide excision repair in Drosophila and S2 cells.

Project description:We report the application of single-molecule-based sequencing technology (XR-seq) for high-throughput profiling of nucleotide excision repair in Drosophila four developmental stages and S2 cells. By obtaining over six billion bases of sequence from UV and cisplatin damage antibodies immunoprecipitated excision DNA, we generated genome-wide nucleotide excision repair maps of Drosophila Embryo, Larva, Pupa , two gender of adults and S2 cells . We find that Drosophila performs transcription-coupled repair (TCR) at all its developmental stages. S2 cell carry out TCR response to both UV and Cisplatin damage. Finally, we show that XPC repair factor is required for both global and transcription-coupled repair in Drosophila. This study provides the mechanism of nucleotide excision repair of Drosophila in vivo and vitro response to UV and Cisplatin damage.

2022-02-25 | GSE184926 | GEO

Transcriptional analysis of nucleotide excision repair defects

Project description:Transcriptional analysis of nucleotide excision repair defects

| PRJNA714383 | ENA