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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

SUBMITTER: Elisabeth Martinez

PROVIDER: E-GEOD-46632 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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A small molecule modulates Jumonji histone demethylase activity and selectively inhibits cancer growth.

Wang Lei L Chang Jianjun J Varghese Diana D Dellinger Michael M Kumar Subodh S Best Anne M AM Ruiz Julio J Bruick Richard R Peña-Llopis Samuel S Xu Junjie J Babinski David J DJ Frantz Doug E DE Brekken Rolf A RA Quinn Amy M AM Simeonov Anton A Easmon Johnny J Martinez Elisabeth D ED

Nature communications 20130101

The pharmacological inhibition of general transcriptional regulators has the potential to block growth through targeting multiple tumorigenic signalling pathways simultaneously. Here, using an innovative cell-based screen, we identify a structurally unique small molecule (named JIB-04) that specifically inhibits the activity of the Jumonji family of histone demethylases in vitro, in cancer cells, and in tumours in vivo. Unlike known inhibitors, JIB-04 is not a competitive inhibitor of α-ketoglut ...[more]

PMID: 23792809

Similar Datasets

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.

2013-07-08 | GSE46632 | GEO

Targeting Focal Adhesion Kinase overcomes erlotinib resistance in smoke induced lung cancer by altering phosphorylation of Epidermal Growth Factor Receptor

Project description:Cigarette smoking is the leading cause for non-small cell lung carcinoma (NSCLC). Tyrosine kinase inhibitors (TKIs) targeting EGFR are in clinical practice and has benefitted patients with EGFR mutations. However, EGFR based targeted therapies have shown limited success in smokers. Identification of alternate signaling mechanism(s) leading to TKI resistance in smokers is critical for developing novel therapies for lung cancer. We observed increased resistance to erlotinib in H358 lung cancer cells exposed to cigarette smoke (H358-S) compared to parental cells. To systematically identify signaling pathways that could potentially confer resistance to erlotinib, we carried out stable isotope labeling by amino acids in cell culture (SILAC)-based phosphotyrosine analysis of H358-S and parental cells. We identified 238 unique phosphosites, of which 111 phosphosites were hyperphosphorylated (≥ 2-fold¬¬¬¬¬¬) in H358 -S cells. Importantly, we observed hyperphosphorylation of EGFR at Y1197 and non-receptor tyrosine kinases, including FAK and FRK in H358-S cells. Inhibition of FAK with its inhibitor PF-562271 led to decreased cellular proliferation and invasive ability of the smoke exposed cells. Further, we observed that treatment with PF-562271 could restore dependency of H358-S cells on EGFR signaling.

2018-03-21 | PXD006705 | Pride

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

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

Gene expression profiling of NSCLC cell lines upon TGFb-induced epithelial-mesenchymal transition (EMT)

Project description:Epithelial-mesenchymal transition has been implicated in tumor metastasis, cancer drug resistance and cancer stem cell features. In this study, we examined gene expression profiles of three non-small cell lung cancer cell lines, before and after experimentally induced EMT. We modeled epitheial-mesenchyml transition by culturing A549, HCC827 and NCI-H358 cells in the presence of TGFb for three weeks, and compared gene expression profiles of the paretnal cells and cells after EMT.

2014-11-19 | E-GEOD-49644 | 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

p21-Activated kinase 6 (PAK6) is associated with enhanced proliferation in lung cells exposed chronically to cigarette smoke

Project description:Epidemiological data clearly establishes cigarette smoking as one of the major cause for lung cancer worldwide. There is no standard screening method for lung cancer even in high-risk populations and the overall five-year survival has not changed significantly in the last decade. First-line treatment for lung cancer includes surgical resection, chemotherapy, and radiation. Recently with the advancement of systems biology, targeted therapy has become one of the most preferred modes of treatment for cancer. Though certain targeted therapies such as anti-EGFR are in clinical practice, they have shown limited success in the smokers suffering from lung cancer. This demands the discovery of alternative drug targets through systematic investigation of altered signaling mechanisms. To study dysregulated signaling pathways due to chronic cigarette smzoke exposure, we carried out SILAC-based phosphoproteome analysis of lung cell line H358 chronically exposed to cigarette smoke. We identified 1,812 phosphosites, of which 278 were hyperphosphorylated (≥ 3-fold) in the H358 cells exposed to cigarette smoke. We identified several known and some novel kinases and key signaling molecules that were hyperphosphorylated in response to chronic exposure to cigarette smoke

2016-12-14 | PXD003108 | Pride

Comparison of gene expression in control and BRG1-knockdown H358 cell lines

Project description:Transcription was assessed in the human H358 NSCLC cell line after knockdown of BRG1, one of the mutually exclusive subunits of the SWI/SNF chromatin remodeling complex, by 2 different shRNAs. One biolgical replicate of each treatment; 4 technical replicates of each treatment.

2014-09-23 | E-GEOD-58542 | biostudies-arrayexpress

Effect of SRSF2 over-expression in a human lung carcinoma cell line

Project description:We showed that the over-expression of the SR protein SRSF2 led to the regulation of transcript abundance of many genes. H358 cell line with 6 samples with SRSF2 over-expression and 6 samples as control.

2013-08-30 | E-GEOD-50467 | biostudies-arrayexpress

Malaria Hepatocyte HC-04.J7 Project

Project description:Characterization of three hepatocyte cell lines (2 parental and 1 clone), under two different media conditions. Parental cell lines HepG2 and HC-04, single cell cloned from HC-04 defined as HC-04.J7. The goal of the project initially was to investigate the invasion of hepatocytes by Plasmodium falciparum sporozoites, and once found that the HC-04 cell had a higher invasion than HepG2, single cell isolates were generated from HC-04 before being expanded. The resulting HC-04.J7 isolate further improved the invasion rate. Transcriptomic and proteomic data sets were generated from all cell lines in both media, than analyzed for potential receptors or biochemical pathways that play a role in the increased invasion of HC-04 and specifically, HC-04.J7.

2019-11-12 | PXD008613 | Pride

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