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Transcriptomic and epigenomic profiling of H3K27me3 demethylases inhibitor GSK-J4 induced changes in colon cancer cells (ChIP-Seq)

ABSTRACT: Transcriptomic and epigenomic profiling of H3K27me3 demethylases inhibitor GSK-J4 induced changes in colon cancer cells (ChIP-Seq)

PROVIDER: PRJNA611614 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11273568.fastq.gz	Fastqsanger.gz
	SRR11273569.fastq.gz	Fastqsanger.gz
	SRR11273570.fastq.gz	Fastqsanger.gz
	SRR11273571.fastq.gz	Fastqsanger.gz
	SRR11273572.fastq.gz	Fastqsanger.gz

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Transcriptomic and epigenomic profiling of H3K27me3 demethylases inhibitor GSK-J4 induced changes in colon cancer cells

Project description:Transcriptomic and epigenomic profiling of H3K27me3 demethylases inhibitor GSK-J4 induced changes in colon cancer cells

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Transcriptomic and epigenomic profiling of H3K27me3 demethylases inhibitor GSK-J4 induced changes in colon cancer cells (ChIP-Seq)

Project description:H3K27me3 demethylases UTX and JMJD3 play vital roles in development and disease, including cancer. Therefore, we systematically investigated the impact of inhibition of these two demethylases using a small molecule inhibitor in colon cancer cells.

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Transcriptomic and epigenomic profiling of H3K27me3 demethylases inhibitor GSK-J4 induced changes in colon cancer cells (RNA-Seq)

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Transcriptomic and epigenomic profiling of H3K27me3 demethylases inhibitor GSK-J4 induced changes in colon cancer cells (RNA-Seq)

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RNA-seq of GSK-J4 Treated Neuroblastoma Cell Lines

Project description:High-risk neuroblastoma is often distinguished by amplification of MYCN and loss of differentiation potential with tumors refractory to retinoic acid differentiation based therapies. Here, we leverage high-throughput drug screening of epigenetic targeted therapies across a large and diverse tumor cell line panel to uncover the hypersensitivity of neuroblastoma cells to GSK-J4, a small molecule dual inhibitor of H3K27 demethylases UTX and JMJD3. Mechanistically, GSK-J4 induced neuroblastoma differentiation and ER stress with accompanying upregulation of PUMA and apoptosis induction. Retinoic acid (RA)-resistant neuroblastoma cells were sensitive to GSK-J4. Additionally, GSK-J4 was effective at blocking the growth of chemorefractory and patient-derived xenograft models of high-risk neuroblastoma in vivo. Further, GSK-J4 and RA combined to induce differentiation, ER-stress and limit the growth of neuroblastomas resistant to either drug alone. In MYCN-amplified neuroblastoma, which is the most prevalent driver gene alteration in the refractory population, PUMA induction by GSK-J4 sensitized tumors to the BCL-2 inhibitor venetoclax, demonstrating that epigenetic targeted therapies and BH3 mimetics can be rationally combined to treat high-risk subset of neuroblastoma. Therefore, H3K27 demethylation inhibition is a promising therapeutic target to treat high-risk neuroblastoma, and H3K27 demethylation can be part of rational combination therapies to induce robust anti-neuroblastoma activity.

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Expression data from neuroblastoma cells treated with GSK-J4 or KTP-330

Project description:Neuroblastoma (NB) is a common pediatric malignancy tumor with poor outcome. Recent studies show that GSK-J4, an inhibitor of lysine 27 of histone 3 (H3K27) demethylases, and KTP-330, a clinically available inhibitor of XPO1 protein, are promising anti-cancer agents. However, their molecular mechanisms in neuroblastoma are still unclear. In this study, we used microarrays to analyze the global change in gene expression as a result of GSK-J4 or KTP-330 treatment in the human neuroblastoma cell line SH-SY5Y.

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