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Genome-wide ChIP-Seq from GSK-J4 or siKDM6B-treated lung adenocarcinoma cell line A549

ABSTRACT: Genome-wide ChIP-Seq from GSK-J4 or siKDM6B-treated lung adenocarcinoma cell line A549

PROVIDER: PRJNA553220 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9654260.fastq.gz	Fastqsanger.gz
	SRR9654261.fastq.gz	Fastqsanger.gz
	SRR9654262.fastq.gz	Fastqsanger.gz
	SRR9654256.fastq.gz	Fastqsanger.gz
	SRR9654257.fastq.gz	Fastqsanger.gz

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Genome-wide RNA-seq from GSK-J4-treated lung adenocarcinoma cell lines

Project description:Purpose: The goals of our study were to identify downstream pathway regulated by GSK-J4 in lung adenocarcinoma Methods: RNAs isolated from GSK-J4-treated or untreated lung adenocarcinoma (HCC827, H23 and A549) were analyzed by using an Illumina Nextseq500 Conclusions: Our study represents the first detailed transcriptomic analysis of effects of GSK-J4 in lung adenocarcinoma.

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Genome-wide ChIP-Seq from GSK-J4 or siKDM6B-treated lung adenocarcinoma cell line A549

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Jumonji Demethylase Inhibitor GSK-J4 treated Multiple Myeloma JJN3 and RPMI

Project description:Analysis of Multiple Myeloma Cell lines JJN-3 and RPMI gene expression following treated with GSK-J4 or Bortezomib Total RNA extracted from cells after 6 or 24 hour treatment with either GSK-J4, GSK-J5, Bortezomib or vehicle

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Genome-wide assessment of GSK-J4-treated lung adenocarcinoma cell lines

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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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Genome-wide RNA-seq from GSK-J4-treated lung adenocarcinoma cell lines

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Project description:Thioneins are cysteine-rich, evolutionary conserved apoproteins that regulate divalent metal homeostasis by virtue of their metal-chelation properties resulting in the ligand-bound metallothionein state. Previous studies have demonstrated a transient upregulation (102- 103-fold) of a cluster of metallothionein genes as part of a transcriptional response to a class of histone demethylase tool compounds targeting human Fe2+ dependent ketoglutarate oxygenases KDM6A (UTX) and KDM6B (JmjD3). Exposure of multiple myeloma cells to the prototypic bioactive KDM6 inhibitor GSK-J4 induces apoptotic cell death and transcriptomic profiles that are dominated by metal and metabolic stress response signatures. We here investigate the hypothesis that the metal-chelating property of GSK-J4 provides the means for transport and intracellular release of Zn2+ leading to a metallothionein transcriptomic response signature. Live cell imaging upon myeloma cell exposure to GSK-J4 shows a transient increase of intracellular free Zn2+ concentrations upon KDM6 inhibitor treatment consistent with a model of inhibitor mediated metal transport. Comparison of KDM6 inhibitor and ZnSO4 treatments in the presence or absence of metal chelators show that both treatment conditions induce different transcription factor repertoires with an overlapping MTF1 transcriptional regulation responsible for metallothionein and metal ion transport regulation.

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