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Transcriptome change mediated by tumor-intrinsic PRC2 inactivation in transplant murine breast cancer AT3 tumor model in C57BL/6J mice

ABSTRACT: Transcriptome change mediated by tumor-intrinsic PRC2 inactivation in transplant murine breast cancer AT3 tumor model in C57BL/6J mice

PROVIDER: PRJNA744572 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15067142.fastq.gz	Fastqsanger.gz
	SRR15067143.fastq.gz	Fastqsanger.gz
	SRR15067144.fastq.gz	Fastqsanger.gz
	SRR15067145.fastq.gz	Fastqsanger.gz
	SRR15067146.fastq.gz	Fastqsanger.gz

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Transcriptome change mediated by tumor-intrinsic PRC2 inactivation in transplant murine breast cancer AT3 tumor model in C57BL/6J mice

Project description:We used CRISPR/Cas9-mediated knockout of PRC2 core components, Eed and generated PRC2-isogenic murine mammary tumor model (AT3, sgCon vs. sgEed ) amenable for syngeneic transplant in C57BL/6J mice. Transcriptome analysis of the explanted PRC2-wt (sgCon) and PRC2-loss (sgEed) AT3 tumors by RNA-seq demonstrated that PRC2 loss led to the upregulation of various developmental pathways, and the downregulation of both innate and adaptive immune response pathways.

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Single-cell transcriptional profiles of BM, PB and lung neutrophils from naïve (C57BL/6J), AT3, and AT3-gcsf tumor-bearing mice

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Project description:The methyltransferase Polycomb Repressive Complex 2 (PRC2), composed of EZH2, SUZ12, and EED subunits, is associated with transcriptional repression via tri-methylation of histone H3 on lysine 27 residue (H3K27me3). PRC2 is a validated drug target, as the EZH2 gain-of-function mutations identified in patient samples drive tumorigenesis. PRC2 inhibitors have been discovered and demonstrated anti-cancer efficacy in clinic. However, their pharmacological mechanisms are poorly understood. MAK683 is a potent EED inhibitor in clinical development. The overall goal of our study is to understand the molecular events leading to tumor regression after PRC2 inhibition. Our study revealed that multiple senescence-associated secretory phenotype (SASP) genes, such as Gata4, Mmp2/10, Itga2 and Gbp1, are derepressed upon PRC2 inhibition and contribute to decreased Ki67+, ECM reorganization, inflammation and tumor regression even in Cdkn2a/p16 knockout tumor.

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