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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE179345 | GEO | 2022/08/03

REPOSITORIES: GEO

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Transcriptome analysis by RNA sequencing after treatment with JIB-04 in colorectal cancer

Project description:We investigate RNA sequencing analysis revealed that the JIB-04 treatment altered the expression of genes that are involved in the cell cycle, apoptosis, and DNA replication and are also related to several cancers including colorectal cancer. JIB-04 also altered the expression of genes involved in various signaling pathways such as the MAPK signaling pathway, the PI3K-Akt signaling pathway, and the Wnt signaling pathway, which is crucial for the proliferation and maintenance of colorectal cancer cells.

2018-11-01 | GSE106407 | 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

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

2013-07-08 | GSE46632 | GEO

RNA-Seq analysis of JIB-04 effects on global cellular transcription and HIV in 2D10 T cells

Project description:Measuring the effects of the compound JIB-04 on global transcription, NFkB pathway-related genes, and integrated HIV proviral DNA.

2018-05-16 | GSE109460 | 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

RNA sequencing data of 2102EP cells treated with epigenetic agents Quisinostat, JIB-04, Chaetocin, MZ-1, LP99, PRT4165 and GSK343 and DMSO as solvent control

Project description:Single end 3' RNA sequencing of embryonal carcinoma cell line 2102EP treated with epigenetic agents Quisinostat, JIB-04, Chaetocin, Mz-1, LP99, PRT4165 and GSK343. DMSO was used as solvent control. Cells were treated with the epi-drugs for 16 h.

2022-01-21 | GSE189472 | GEO

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

Transcription analysis from the human embryonic kidney 293 cells (HEK293) were pre-treated with JIB-04, and then uninfected and infected with porcine rotavirus (PoRV)

Project description:Purpose: Investigation of whole genome gene expression level changes in HEK293 cells response to JIB-04 and porcine rotavirus (PoRV)

2020-08-14 | GSE156219 | GEO

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

Transcriptomic and Proteomic Response of HC-04 to hepatocyte growth factor (HGF)

Project description:The routine study of human malaria liver-stage biology in vitro is hampered by low infection efficiency of human hepatocellular carcinoma (HCC) lines (<0.1%), poor understanding of steady-state HCC biology, and lack of appropriate tools for trace sample analysis. HC-04 is the only HCC that supports complete development of human malaria parasites. We hypothesized that HCCs are in various intermediate stages of the epithelial-mesenchymal transition (EMT) and HC-04s retain epithelial characteristics that permit infection. We developed an novel analytical approach to test this hypothesis viz. the HC-04 response to hepatocyte growth factor (HGF). We used online two-dimensional liquid chromatography tandem mass spectrometry (2D-LC-MS/MS) to quantify protein expression profiles in HC-04 pre-/post-HGF treatment and validated these results by RT-qPCR and microscopy. We successfully increased protein identification efficiency over offline-2D methods by 12-fold using less sample material, allowing robust protein quantification. We observed expected up-regulation and down-regulation of EMT protein markers in response to HGF, but also unexpected cellular responses. HC-04 is thus susceptible to HGF-mediated signaling but to a lesser degree than what we observed for HepG2, a widely used, but poor malaria HCC model. Our analytical approach to understanding the basic biology of HC-04 helps us understand the factors that may influence its utility as a model for malaria liver-stage development. We observed that HC-04 treatment with HGF prior to the addition of Plasmodium falciparum sporozoites did not facilitate cell invasion, arguing for unlinking the effect of HGF on malaria liver stage development from hepatocyte invasion. Finally, our 2D-LC-MS/MS approach and broadly applicable experimental strategy should prove useful in the analysis of various hepatocyte-pathogen interactions, tumor progression and early disease events.

2014-02-17 | PXD000682 | Pride

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