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KDM4A regulated genes in human squamous carcinoma cells

ABSTRACT: To establish a robust cellular model system for screening genes associated with cell invasion, we over-expressed the oncogenic translocated promoter region (Tpr)-MET proteins in SCC23 cells (SCC23/MET). Using a functional siRNA screen, we identified that the histone demethylase KDM4A played a critical role in the invasive growth and metastasis of SCC mediated by the Oncogenic MET. To investigate the molecular mechanism through which KDM4A inhibit the tumor cell invasion, we knock-down KDM4A in SCC23/MET cell and performed a gene microarray to examine which genes may be regulaged by kDM4A.

ORGANISM(S): Homo sapiens

PROVIDER: GSE44238 | GEO | 2013/05/03

SECONDARY ACCESSION(S): PRJNA189228

REPOSITORIES: GEO

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KDM4A regulated genes in human squamous carcinoma cells

Project description:To establish a robust cellular model system for screening genes associated with cell invasion, we over-expressed the oncogenic translocated promoter region (Tpr)-MET proteins in SCC23 cells (SCC23/MET). Using a functional siRNA screen, we identified that the histone demethylase KDM4A played a critical role in the invasive growth and metastasis of SCC mediated by the Oncogenic MET. To investigate the molecular mechanism through which KDM4A inhibit the tumor cell invasion, we knock-down KDM4A in SCC23/MET cell and performed a gene microarray to examine which genes may be regulaged by kDM4A. We generated two stable cell lines. one was infected with virus containing scramble and another infected with virus infected with virus containing KDM4A shRNA. Total RNA were extracted from these two cell lines and subject to microarray.

2013-05-03 | E-GEOD-44238 | biostudies-arrayexpress

Histone demethylase KDM4A-mediated promotion of PAF1/NFATC2 expression is required for oncogenesis in MLL-AF9 acute myeloid leukemia [ChIP-seq]

Project description:In this study we identified the histone demethylase KDM4A as an essential and selective regulator of AML oncogenic potential. ChIPseq was used to identify KDM4A bound genes and follow changes in H3K9me2/3 and H3K27me3 following KDM4A knockdown in MLL-AF9 human AML THP-1 cells

2021-01-17 | GSE125375 | GEO

Histone demethylase KDM4A-mediated promotion of PAF1/NFATC2 expression is required for oncogenesis in MLL-AF9 acute myeloid leukemia [RNA-seq]

Project description:In this study we identified the histone demethylase KDM4A as an essential and selective regulator of AML oncogenic potential. RNAseq was used to follow the changes in gene expression following KDM4A knockdown in MLL-AF9 human AML THP-1 cells

2021-01-17 | GSE125374 | GEO

KDM4A regulated gene expression in human prostate cancer LNCaP cell

Project description:Histone lysine demethylase KDM4A is overexpressed in prostate cancer and plays a crucial role in tumor growth and survival. To understand the mechanisms underlying KDM4A-depedent cell growth and survival, microarray analysis was performed in LNCaP cells transduced with control or KDM4A specific-knockdown construct. The role of KDM4A in prostate carcinogenesis involves activation of E2F1 and androgen receptor transcriptional profiles. LNCaP cells were transduced by lentivirus carrying control pLKO.1 (empty vector) or shKDM4A construct (KDM4A-specific shRNA) for three days, followed by RNA extraction. Affymetrix GeneChip Human Genome U133 Plus 2.0 Arrays were used for microarray analysis.

2016-07-26 | E-GEOD-77928 | biostudies-arrayexpress

KDM4A regulated gene expression in human prostate cancer LNCaP cell

2016-07-26 | GSE77928 | GEO

2.5 dpc Uterus Chip-Seq of Kdm4a mice

Project description:Purpose: ChipSeq allows us to identify binding sites of target proteins of interest in the genome, helping create a global profile for the same. Kdm4a is a H3K9me3 histone demethylase that acts to prevent spurious accumulation of this repressive mark at H3K4me3 positive transcription start sites. To complement transcriptome data from Kdm4a mice, we performed Chip-Seq on 2.5dpc mouse uterus of 8-10 week old littermate control and Kdm4a knockout mice for Kdm4a, H3K9me3 and H3K4me3. This would help us check which of the target genes with changed gene expression was due to the direct change in histone lanscape in absence of Kdm4a.

2017-08-17 | GSE96591 | GEO

Targeting KDM4A epigenetically activates tumor cell-intrinsic immunity and overcomes resistance to PD1 blockade in squamous cell carcinoma by inducing DNA replication stress

Project description:To investigate the mechanisms by which KDM4A knockout ameliorates the invasive growth and metastasis of primary mouse squamous cell carcinoma (SCC), we isolated fresh SCCs from tumor cell-specific KDM4A knockout and control mice, and then did the whole transcriptome analysis using RNA-Seq. Results showed that KDM4A knockout stimulated anti-tumor immunity.

2021-03-23 | GSE137953 | GEO

Efficient Elimination of Acute Myeloid Leukaemia Cells through Inhibition of KDM4A

Project description:We previously identified an essential role for the H3K9me3 histone demethylase, KDM4A, in maintaining AML cell survival, with genetic depletion by shRNA of KDM4A inducing leukaemic cell death with little effect on normal haematopoiesis. We hypothesised KDM4A inhibition may represent a novel and effective strategy to treat AML. To address this, we provided proof-of-principle for the use of KDM4 inhibitors (KDM4Ai) and fully characterised their functional potential in AML cells and identified the epigenetic mechanisms underpinning the essential role of KDM4A activity in THP-1 cells using both ChIP-seq and RNA-seq, delineating and functionally validating the epigenomic network regulated by KDM4A, showing that selective loss of KDM4A is sufficient to induce apoptosis in a broad spectrum of human AML cells. This detrimental phenotype results from a global accumulation of H3K9me3 and H3K27me3 at KDM4A targeted genomic loci thereby causing down-regulation of a KDM4A-PAF1 controlled transcriptional program essential for leukemogenesis, distinct from that of KDM4C.

2022-12-31 | GSE173995 | GEO

Promoter-specific recruitment of PPARG in adipocytes depends on GPS2-dependent stabilization of histone demethylase KDM4A/JMJD2 [KDM4A]

Project description:Timely and selective recruitment of transcription factors to their appropriate DNA-binding sites represents a critical step in regulating gene activation; however the regulatory strategies underlying each factor’s effective recruitment to specific promoter and/or enhancer regions are not fully understood. Here, we identify an unexpected regulatory mechanism by which promoter-specific binding, and therefore function, of PPARG in adipocytes requires G protein Suppressor 2 (GPS2) to prime the local chromatin environment via inhibition of the ubiquitin ligase RNF8 and stabilization of the H3K9 histone demethylase KDM4A/JMJD2. Integration of genome-wide profiling data indicates that the pioneering activity of GPS2/KDM4A is required for PPARG mediated regulation of a specific transcriptional program, including the lipolytic enzymes ATGL and HSL. Hence, our findings reveal that GPS2 exerts a biologically important function in adipose tissue lipid mobilization by directly regulating ubiquitin signaling and indirectly modulating chromatin remodeling to prime selected genes for activation.

2014-07-14 | GSE57778 | GEO

The lysine demethylase KDM4A controls the cell-cycle expression of replicative canonical histone genes

Project description:Chromatin modulation provides a key checkpoint for controlling cell cycle regulated gene networks. The replicative canonical histone genes are one such gene family under tight regulation during cell division. These genes are most highly expressed during S phase when histones are needed to chromatinize the new DNA template. While this fact has been known for a while, limited knowledge exists about the specific chromatin regulators controlling their temporal expression during cell cycle. Since histones and their associated mutations are emerging as major players in diseases such as cancer, identifying the chromatin factors modulating their expression is critical. The histone lysine tri-demethylase KDM4A is regulated over cell cycle and plays a direct role in DNA replication timing, site-specific rereplication, and DNA amplifications during S phase. Here, we establish an unappreciated role for the catalytically active KDM4A in directly regulating canonical replicative histone gene networks during cell cycle. Of interest, we further demonstrate that KDM4A interacts with proteins controlling histone expression and RNA processing. Together, this study provides a new function for KDM4A in modulating canonical histone gene expression.

2021-10-27 | GSE154684 | GEO

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