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Effect of depletion of histone demethylases KDM6A and KDM6B on gene expression in the acute myeloid leukemia (AML) cell line U937 [RNA-seq]

ABSTRACT: Effect of depletion of histone demethylases KDM6A and KDM6B on gene expression in the acute myeloid leukemia (AML) cell line U937 [RNA-seq]

PROVIDER: PRJNA926974 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23203932_1.fastq.gz	Fastqsanger.gz
	SRR23203932_2.fastq.gz	Fastqsanger.gz
	SRR23203933_1.fastq.gz	Fastqsanger.gz
	SRR23203933_2.fastq.gz	Fastqsanger.gz
	SRR23203934_1.fastq.gz	Fastqsanger.gz

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Effect of depletion of histone demethylases KDM6A and KDM6B on gene expression in the acute myeloid leukemia (AML) cell line U937 [RNA-seq]

Project description:To investigate the function of KDM6A and KDM6B in regulating gene expression in AML, we generated U937 cell lines having knockdown of either KDM6A, KDM6B or both using lentiviral shRNA. Control cells were generated using a scrambled shRNA. We then profiled gene expression using RNA-seq data obtained from the 3 knockdown cell lines compared with the control cell line.

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Refractory testicular germ cell tumors are highly sensitive to the targeting of polycomb pathway demethylases KDM6A and KDM6B

Project description:Testicular germ cell tumors (TGCTs) can be treated with cisplatin-based therapy. However, a clinically significant number of cisplatin-resistant patients die from progressive disease as no effective alternatives exist. Curative cisplatin therapy results in acute and life-long toxicities in the young TGCT patient population providing a rationale to decrease cisplatin exposure. In contrast to genetic alterations, recent evidence suggests that epigenetics is a major driving factor for TGCT formation, progression, and response to chemotherapy. Hence, targeting epigenetic pathways with “epidrugs” is one potential relatively unexplored strategy to advance TGCT treatment beyond cisplatin. In this report, we demonstrate for the first time that targeting polycomb demethylases KDM6A and KDM6B with epidrug GSK-J4 can treat both cisplatin-sensitive and -resistant TGCTs. While GSK-J4 had minimal effects alone on TGCT tumor growth in vivo, it dramatically sensitized cisplatin-sensitive and -resistant TGCTs to cisplatin. We validated KDM6A/KDM6B as the target of GSK-J4 since KDM6A/KDM6B genetic depletion had a similar effect to GSK-J4 on cisplatin-mediated anti-tumor activity and transcriptome alterations. Pharmacologic and genetic targeting of KDM6A/KDM6B potentiated or primed the p53-dominant transcriptional response to cisplatin, with also evidence for basal activation of p53. Further, several chromatin modifier genes, including BRD4, lysine demethylases, chromodomain helicase DNA binding proteins, and lysine methyltransferases, were repressed with cisplatin only in KDM6A/KDM6B-targeted cells, implying that KDM6A/KDM6B inhibition sets the stage for extensive chromatin remodeling of TGCT cells upon cisplatin treatment. Our findings demonstrate that targeting polycomb demethylases is a new potent pharmacologic strategy for treating cisplatin resistant TGCTs that warrants clinical development.

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Project description:To interrogate the function of KDM6A and KDM6B in regulating genome accessibility, we generated U937 cell lines having knockdown of either KDM6A, KDM6B or both using lentiviral shRNA. We then profiled chromatin accessibility changes using ATAC-seq data obtained from the 3 knockdown cell lines compared with the wild type cell line.

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H3K27me3 demethylases maintain the transcriptional and epigenomic landscape of the intestinal epithelium [RNA-seq]

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Refractory testicular germ cell tumors are highly sensitive to the targeting of polycomb pathway demethylases KDM6A and KDM6B

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KDM4B- and KDM6B-regulated genes in human mesenchymal stem cell osteogenic differentiation

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KDM4B- and KDM6B-regulated genes in human mesenchymal stem cell osteogenic differentiation

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Inhibition of histone H3K27 demethylases inactivates brachyury (TBXT) and promotes chordoma cell death (ChIP-seq)

Project description:Expression of the transcription factor brachyury (TBXT) is normally restricted to the embryo and its silencing is epigenetically regulated. TBXT promotes mesenchymal transition in a subset of common carcinomas, and in chordoma, a rare cancer showing notochordal differentiation, TBXT acts as a putative oncogene: we hypothesised that TBXT expression could be controlled through epigenetic inhibition to promote chordoma cell death. Screening of five human chordoma cell lines revealed that pharmacological inhibition of the histone 3 lysine 27 demethylases KDM6A (UTX) and KDM6B (JMJD3) leads to cell death. This effect was phenocopied by the dual genetic inactivation of KDM6A/B using CRISPR/Cas9. Inhibition of KDM6A/B using a novel compound, KDOBA67, led to a genome-wide increase in repressive H3K27me3 marks, with concomitant reduction in H3K27ac, H3K9ac and H3K4me3 active marks. We show that TBXT is a KDM6A/B target gene, and that changes in the chromatin at TBXT following KDOBA67 treatment were associated with a reduction in TBXT protein levels in all models tested, including primary patient-derived cultures. KDOBA67 downregulated also the expression of a network of transcription factors critical for chordoma survival, whereas upregulated pathways were dominated by ATF4-driven stress and pro-apoptotic responses in all models. Blocking the AFT4-stress response did not prevent the suppression of TBXT and induction of cell death, but viability was increased by ectopic overexpression of TBXT, therefore implicating TBXT as potential therapeutic target of H3K27 demethylases inhibitors. Our work highlights how knowledge of normal processes in fetal development can provide insight into tumourigenesis and identify novel therapeutic approaches.

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