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Cancer cell type-specific derepression of transposable elements by inhibition of chromatin modifier enzymes [ChIP-Seq]

ABSTRACT: Cancer cell type-specific derepression of transposable elements by inhibition of chromatin modifier enzymes [ChIP-Seq]

PROVIDER: PRJNA1069071 | ENA |

REPOSITORIES: ENA

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			Action	DRS
		Other
	SRR27730568.fastq.gz	Fastqsanger.gz
	SRR27730573.fastq.gz	Fastqsanger.gz
	SRR27730575.fastq.gz	Fastqsanger.gz
	SRR27730581.fastq.gz	Fastqsanger.gz

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Cancer cell type-specific derepression of transposable elements by inhibition of chromatin modifier enzymes

Project description:Cancer cell type-specific derepression of transposable elements by inhibition of chromatin modifier enzymes

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Cancer cell type-specific derepression of transposable elements by inhibition of chromatin modifier enzymes

Project description:Derepression of transposable elements (TE) by epigenetic therapy leads to the activation of immune response in cancer cells. However, the molecular mechanism of TE regulation by distinct chromatin modifier enzymes (CME) in context of p53 is still elusive. Here, we used FDA-approved epigenetic drugs to systematically inhibit distinct CMEs in p53 wild-type and p53-mutant colorectal, esophageal, and prostate cancer cells. We show that distinct TE subfamilies are derepressed by inhibition of different CMEs in cell type-specific manner. Co-inhibition of DNMT and HDAC (DNMTi-HDACi) had the most consistent effect across cancer types. Loss of p53 results in stronger TE activation and TE-chimeric transcript expression and this effect is largely mediated by the non-genomic actions of p53. Robust immune response elicited by DNMTi-HDACi is due to induced inverted repeat Alu expression concomitant with reduced ADAR1-mediated Alu RNA editing. Collectively, our systematic analyses provide insights for rational use of epigenetic therapies in distinct cancers.

2025-06-16 | GSE254244 | GEO

Cancer cell type-specific derepression of transposable elements by inhibition of chromatin modifier enzymes [RNA-Seq]

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Cancer cell type-specific derepression of transposable elements by inhibition of chromatin modifier enzymes [ChIP-Seq]

Project description:The combination of epigenetic and immunotherapy is emerging as a promising approach for cancer therapy. Derepression of transposable elements (TE) by epigenetic drugs leads to activation of immune response. However, the molecular mechanism of TE regulation by distinct chromatin modifier enzymes (CME) in context of p53 is still elusive. Here, we used FDA-approved epigenetic drugs to systematically inhibit distinct CMEs in p53 wild-type and p53-mutant colorectal, esophageal, and prostate cancer cells. We show that distinct TE subfamilies are derepressed by inhibition of different CMEs in cell type-specific manner. Co-inhibition of DNMT and HDAC (DNMTi-HDACi) had the most consistent effect across cancer types. Loss of p53 results in stronger TE activation and TE-chimeric transcript expression and this effect is largely mediated by the non-genomic actions of p53. Robust immune response elicited by DNMTi-HDACi is due to induced inverted repeat Alu expression concomitant with reduced ADAR1-mediated Alu RNA editing, whereas SETDB1 inhibition activates ADAR1 expression. Collectively, our systematic analyses provide insights for rational use of epigenetic therapies in distinct cancers.

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Project description:Pleurotus ostreatus, also known as the oyster mushroom, is an active lignin decomposer in the forests. The genomes of the monokaryotic strains PC15 and PC9 have been used to characterize the content and distribution of transposable elements. This study analyzes the impact of transposable element insertions on the global transcriptome of P. ostreatus. The transcriptome of PC15 and PC9 has been analyzed in exponential growth during submerged fermentation in malt-yeast extract-sucrose medium RNAseq of two P. ostreatus strains: PC15 and PC9

2016-05-19 | E-GEOD-81586 | biostudies-arrayexpress

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