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Transposon-triggered innate immune response confers cancer resistance to the blind mole rat [seq]

ABSTRACT: Transposon-triggered innate immune response confers cancer resistance to the blind mole rat [seq]

PROVIDER: PRJNA751908 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15340401_1.fastq.gz	Fastqsanger.gz
	SRR15340401_2.fastq.gz	Fastqsanger.gz
	SRR15340402_1.fastq.gz	Fastqsanger.gz
	SRR15340402_2.fastq.gz	Fastqsanger.gz
	SRR15340403_1.fastq.gz	Fastqsanger.gz

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Transposon-triggered innate immune response confers cancer resistance to the blind mole rat

Project description:Transposon-triggered innate immune response confers cancer resistance to the blind mole rat

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Transposon-triggered innate immune response confers cancer resistance to the blind mole rat [array]

Project description:Blind mole rats (BMRs) are small rodents, characterized by exceptionally long lifespan (> 21 years) and resistance to both spontaneous and induced tumorigenesis. Here we report that cancer resistance in the BMR is mediated by retrotransposable elements (RTEs). BMR cells and tissues express very low levels of DNA methyltransferase 1 (DNMT1). Upon cell hyperplasia, the BMR genome DNA loses methylation, resulting in activation of RTEs. Up-regulated RTEs form cytoplasmic RNA/DNA hybrids, which activate cGAS-STING pathway to induce cell death. Although this mechanism is enhanced in the BMR, we show that it functions in mice and human. We propose that RTEs were coopted to serve as tumor suppressors that monitor cell proliferation and are activated in premalignant cells to trigger cell death via activation of innate immune response. RTEs activation is a double-edged sword, serving as a tumor suppressor but in late life contributing to aging via induction of sterile inflammation.

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Transposon-triggered innate immune response confers cancer resistance to the blind mole rat [seq]

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Transposon-triggered innate immune response confers cancer resistance to the blind mole rat.

Project description:Blind mole rats (BMRs) are small rodents, characterized by an exceptionally long lifespan (>21 years) and resistance to both spontaneous and induced tumorigenesis. Here we report that cancer resistance in the BMR is mediated by retrotransposable elements (RTEs). Cells and tissues of BMRs express very low levels of DNA methyltransferase 1. Following cell hyperplasia, the BMR genome DNA loses methylation, resulting in the activation of RTEs. Upregulated RTEs form cytoplasmic RNA-DNA hybrids, which activate the cGAS-STING pathway to induce cell death. Although this mechanism is enhanced in the BMR, we show that it functions in mice and humans. We propose that RTEs were co-opted to serve as tumor suppressors that monitor cell proliferation and are activated in premalignant cells to trigger cell death via activation of the innate immune response. Activation of RTEs is a double-edged sword, serving as a tumor suppressor but contributing to aging in late life via the induction of sterile inflammation.

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Transposon-triggered innate immune response confers cancer resistance to the blind mole rat

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