Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA201334 | ENA |
REPOSITORIES: ENA
Similar Datasets
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
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
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
Project description:41 lung adenocarcinoma from never-smokers hybridized on Illumina SNP arrays on 13 HumanCNV370-Quadv3 chips. High-resolution array comparative genomic hybridization analysis of lung adenocarcinoma in 41 never smokers for identification of new minimal common regions (MCR) of gain or loss. The SNP array analysis validated copy-number aberrations and revealed that RB1 and WRN were altered by recurrent copy-neutral loss of heterozygosity.The present study has uncovered new aberrations containing cancer genes. The oncogene FUS is a candidate gene in the 16p region that is frequently gained in never smokers. Multiple genetic pathways defined by gains of MYC, deletions of RB1 and WRN or gains on 7p and 7q are involved in lung adenocarcinoma in never smokers. A 'Cartes d'Identite des Tumeurs' (CIT) project from the French National League Against Cancer (http://cit.ligue-cancer.net) 41 samples hybridized on Illumina SNP arrays. Submitter : Fabien PETEL petelf@ligue-cancer.net . Project leader : Pr Pierre FOURET pierre.fouret@psl.aphp.fr
2011-07-28 | E-TABM-1169 | biostudies-arrayexpress
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
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
Project description:Evaluation of HIPK2-modulated genes in cancer cells.
| PRJNA144703 | ENA
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
Project description:Transcriptome analysis of ovarian cancer OVSAHO cells treated with JIB-04 and cells transfected with siRNA targeting MECOM
| PRJNA1183650 | ENA
Project description:Small-cell lung cancer (SCLC) arises from neuroendocrine cells within the lung. Along with deletion or loss of function Rb and TP53 mutations, which occur in almost all cases, subsets of SCLC are driven by specific transcription factors including ASCL1, NEUROD1, POU2F3, or YAP1. Various MYC family members provide further inter-tumor heterogeneity. Despite this heterogeneity in SCLC, current treatment for SCLC is subtype agnostic. Although most patients are initially responsive to first line etoposide and platin chemotherapy they soon develop resistance with no effective second line therapy. A recent large NCI screen showed that over 60 SCLC cell line models responded to 500+ investigational drugs in a manner highly correlated with etoposide responses, suggesting none of these drugs would provide benefit for SCLC therapy beyond current chemotherapy. By analyzing publicly available data of shRNA and CRISPR screens in addition to our own RNA-seq expression data we identified KDM4A as a potential candidate to target in SCLC. To underscore the potential of KDM4A as an anti-SCLC target, we tested chemotherapy drug and three JmjC KDM inhibitors across a panel of SCLC cell lines representing all the SCLC transcription factor subtypes and found that SCLC responses to JmjC KDM inhibitors do not correlate to their responses to chemotherapy. Furthermore, we found upon treatment with pan-JmjC KDM inhibitor, JIB-04, many genes in the ER stress signaling pathways are upregulated in SCLC lines, suggesting this is the mechanistic path leading to SCLC slower growth or death. Additionally, analysis found that JIB-04 resistant cells activate pro-survival pathways such as mTOR to perhaps overcome the effects of JIB-04 treatment. Furthermore, the loss of KDM4A in SCLC cell line led to slower proliferation and activity in the ER stress signaling pathway.
2024-10-10 | GSE208446 | GEO