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Global transcriptional response of P. falciparum NF54 early gametocytes treated with the Jumonji histone demethylase inhibitor JIB-04

ABSTRACT: Global transcriptional response of P. falciparum NF54 early gametocytes treated with the Jumonji histone demethylase inhibitor JIB-04

PROVIDER: PRJNA685166 | ENA |

REPOSITORIES: ENA

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Global transcriptional response of P. falciparum NF54 early gametocytes treated with the Jumonji histone demethylase inhibitor JIB-04

Project description:Global transcriptomic profiling of JIB-04 treated and untreated control early gametocytes to determine the downstream effects of Jumonji histone demethylase inhibition on development

2021-04-20 | GSE163189 | GEO

RNAseq of Plasmodium falciparum 3D7 parasites treated with the Jumonji pan inhibitor JIB-04

Project description:Little is known about the role of the three Jumonji C (JmjC) enzymes in Plasmodium falciparum (Pf). Here, we show that JIB-04 and other established inhibitors of mammalian JmjC histone demethylases kill asexual blood stage parasites and are even more potent at blocking gametocyte development and gamete formation. In late stage parasites, JIB-04 increased levels of trimethylated lysine residues on histones, suggesting the inhibition of P. falciparum Jumonji demethylase activity. These epigenetic defects coincide with deregulation of invasion, cell motor, and sexual development gene programs, including gene targets coregulated by the PfAP2-I transcription factor and chromatin-binding factor, PfBDP1. Mechanistically, we demonstrate that PfJmj3 converts 2-oxoglutarate to succinate in an iron-dependent manner consistent with mammalian Jumonji enzymes, and this catalytic activity is inhibited by JIB-04 and other Jumonji inhibitors. Our pharmacological studies of Jumonji activity in the malaria parasite provide evidence that inhibition of these enzymatic activities is detrimental to the parasite.

2020-07-12 | GSE117307 | GEO

Identification of genes modulated by JIB-04 in lung cancer cells

Project description:JIB-04 is an inhibitor of Jumonji histone demethylases identified through a cell based screen that measures the reactivation of an epigenetically silenced transgene. The active JIB-04 E-isomer shows selectivity for cancer vs. normal cells affecting both transcriptional patterns and cell viability in a cancer specific manner. H358 lung cancer cells or the patient matched HCC4017 (cancer) vs. HBEC30KT (immortalized normal) lung cell pair were treated with DMSO vehicle or 500nM E-isomer or 500 nM Z-isomer of JIB-04 for 4 h or 24 h and RNA extracted.

2013-07-08 | E-GEOD-46632 | biostudies-arrayexpress

The Jumonji-domain histone demethylase inhibitor JIB-04 deregulates oncogenic programs and increases DNA damage in Ewing Sarcoma, resulting in impaired cell proliferation and survival, and reduced tumor growth

Project description:The overall goal of this study was to characterize the activity and mechanism(s) of action of the pan-Jumonji domain histone demethylase small molecule inhibitor JIB-04 in the pediatric bone and soft tissue cancer Ewing Sarcoma.

2019-01-03 | GSE119832 | GEO

Identification of genes modulated by JIB-04 in lung cancer cells

2013-07-08 | GSE46632 | GEO

JIB-04, a histone demethylase Jumonji C domain inhibitor, regulates phenotypic switching of vascular smooth muscle cells.

Project description:BackgroundVascular smooth muscle cell (VSMC) phenotype switching is critical for neointima formation, which is the major cause of restenosis after stenting or coronary artery bypass grafting. However, the epigenetic mechanisms regulating phenotype switching of VSMCs, especially histone methylation, are not well understood. As a main component of histone lysine demethylases, Jumonji demethylases might be involved in VSMC phenotype switching and neointima formation.Methods and resultsA mouse carotid injury model and VSMC proliferation model were constructed to investigate the relationship between histone methylation of H3K36 (downstream target molecule of Jumonji demethylase) and neointima formation. We found that the methylation levels of H3K36 negatively correlated with VSMC proliferation and neointima formation. Next, we revealed that JIB-04 (a pan-inhibitor of the Jumonji demethylase superfamily) could increase the methylation levels of H3K36. Furthermore, we found that JIB-04 obviously inhibited HASMC proliferation, and a cell cycle assay showed that JIB-04 caused G2/M phase arrest in HASMCs by inhibiting the phosphorylation of RB and CDC2 and promoting the phosphorylation of CHK1. Moreover, JIB-04 inhibited the expression of MMP2 to suppress the migration of HASMCs and repressed the expression of contraction-related genes. RNA sequencing analysis showed that the biological processes associated with the cell cycle and autophagy were enriched by using Gene Ontology analysis after HASMCs were treated with JIB-04. Furthermore, we demonstrated that JIB-04 impairs autophagic flux by downregulating STX17 and RAB7 expression to inhibit the fusion of autophagosomes and lysosomes.ConclusionJIB-04 suppresses the proliferation, migration, and contractile phenotype of HASMCs by inhibiting autophagic flux, which indicates that JIB-04 is a promising reagent for the treatment of neointima formation.

| S-EPMC9375951 | biostudies-literature

RNAseq of Plasmodium falciparum 3D7 parasites treated with the Jumonji pan inhibitor JIB-04

Project description:RNAseq of Plasmodium falciparum 3D7 parasites treated with the Jumonji pan inhibitor JIB-04

| PRJNA481730 | ENA

Global transcriptomic changes in P. falciparum NF54 gametocytes treated with the histone demethylase inhibitor ML324

Project description:Global transcriptomic profiling of ML324 treated and untreated control gametocytes to determine the downstream effects of histone methyltransferase inhibition on gametocyte development

2020-11-12 | GSE157420 | GEO

Global transcriptomic changes in P. falciparum NF54 gametocytes treated with the histone demethylase inhibitor ML324

Project description:Global transcriptomic changes in P. falciparum NF54 gametocytes treated with the histone demethylase inhibitor ML324

| PRJNA661266 | ENA

Transcriptome analysis by RNA sequencing after treatment with JIB-04 in hepatocellular carcinoma

Project description:Our RNA sequencing analysis revealed that the JIB-04 treatment altered the expression of genes that are involved in the cell cycle, p53 signaling pathway, and apoptosis, and are also related to several cancers including hepatocellular carcinoma. JIB-04 also altered the expression of genes involved in various signaling pathways such as the FoxO signaling pathway, the PI3K-Akt signaling pathway, which is crucial for the proliferation and maintenance of hepatocellular carcinoma cells.

2022-08-03 | GSE179345 | GEO

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