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The KDM1A and KDM7A lysine demethylases cooperate to regulate androgen receptor function in prostate cancer cells [siKMD1A & siKDM7A]

ABSTRACT: KDM1A and KDM7A are Androgen Receptor coregulators. Here siRNAs targeting KDM1A and KDM7A were used to deplete KDM1A and KDM7A in prostate cancer cells and the effect on androgen regulated gene expression and splicing determined.

ORGANISM(S): Homo sapiens

PROVIDER: GSE194280 | GEO | 2026/07/29

REPOSITORIES: GEO

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The KDM1A and KDM7A lysine demethylases cooperate to regulate androgen receptor function in prostate cancer cells [KDM1A & KDM7A inhibitors]

Project description:KDM1A and KDM7A are Androgen Receptor coregulators. Here the KDM1A and KDM7A inhibitors, namoline and TCE-5002 were used to pharmacologically inhibit KDM1A and KDM7A in prosate cancer cells and the effect on androgen regulated gene expression and splicing determined.

2026-07-29 | GSE194279 | GEO

The KDM1A and KDM7A lysine demethylases cooperate to regulate androgen receptor function in prostate cancer cells

Project description:This SuperSeries is composed of the SubSeries listed below.

2026-07-29 | GSE194281 | GEO

The KDM5B and KDM1A lysine demethylases cooperate in regulating androgen receptor expression and signalling in prostate cancer.

Project description: Not available

| S-EPMC10154691 | biostudies-literature

The Lysine Demethylase KDM7A Regulates Immediate Early Genes in Neurons.

Project description:Lysine demethylase KDM7A removes histone modifications H3K9me1/2 and H3K27me1/2. KDM7A plays critical roles in gene expression and contribute to biological processes including tumorigenesis, metabolism, and embryonic development. However, the functions of KDM7A in mammalian nervous system are still poorly explored. In this study, functional roles of KDM7A are comprehensively investigated in neuronal cells by applying CUT&Tag-seq, RNA-seq and mice models. Knockdown of Kdm7a in N2A cells result in the alteration of histone modifications near transcription start sites (TSSs) and the expression changes of a large number of genes. In particular, the expression of immediate early genes (IEGs), a series of genes maintaining the function of the nervous system and associating with neurological disorders, are significantly decreased upon Kdm7a knockdown. Furthermore, in vivo knockdown of Kdm7a in dentate gyrus (DG) neuron of mice hippocampus, via Adeno-associated virus (AAV)-based stereotaxic microinjection, led to a significant decrease of the expression of c-Fos, a marker of neuron activity. Behavior assays in mice further revealed that Kdm7a knockdown in hippocampus repress neuron activity, which leading to impairment of emotion and memory. Collectively, the study reveals that KDM7A affects neuron functions by regulating IEGs, which may provide new clues for understanding epigenetic mechanisms in neurological disorders.

2023-08-21 | GSE232538 | GEO

Illumina Microarray of MRC5 cell with or without KDM7A-DT overexpression

Project description:KDM7A Divergent Transcript (KDM7A-DT) is a stress-induced lncRNAs. In our previous studies, KDM7A-DT showed the most robust cellular phenotype alteration and a significant TP53-dependency upon oxidative and oncogenic stress induction. To investigate the functional roles of KDM7A-DT, we first performed overexpression experiments using fibroblasts. We found that MRC5 cells overexpressing KDM7A-DT escaped cell cycle proliferation and long-term survival ability and were associated with a distinct stress-related morphology (enlarged and flattened cells) compared to cells expressing just the vehicle control. To examine the effects of KDM7A-DT overexpression on the transcriptome, we performed a differential expression gene (DEG) analysis comparing a group of four independent biological replicates of MRC5 overexpressing KDM7A-DT to a group of samples from control cells.

2023-05-01 | E-MTAB-11819 | biostudies-arrayexpress

The lysine demethylase KDM7A regulates immediate early genes in neurons [CUT&Tag]

Project description:There are multiple post-translational modifications on amino acid residues at the N-terminus of histones that affect the structure of chromatin and alter the transcription of genes, thereby regulating a variety of biological processes. Lysine demethylase 7A (KDM7A) mainly removes histone modifications such as H3K9me1/2 and H3K27me1/2. Current research on KDM7A has focused on tumors, metabolism and development, while research on the function of the mammalian nervous system is still lacking. The functions and mechanisms of KDM7A in the regulation of neuronal cell differentiation and cell activity in the nervous system were investigated. Our study found that KDM7A regulates H3K9me2 and H3K27me2 but also affects other inhibitory or active histones, such as H3K9me3 and H3K27ac, thereby disturbing the transcription of some immediate early genes (IEGs) and consequently affecting the differentiation and activity of neuronal cells. IEGs are important for neuron cell proliferation, differentiation, formation of dendrites and neural circuit-related proteins, which are involved in maintaining the normal function of the nervous system. Imbalances in IEG expression have been found in some neurological disorders, such as depression and schizophrenia. Moreover, the changes in various histone modifications in neurodegenerative diseases and brain injury have recently received increasing attention. Therefore, our study provides a basis for revealing the epigenetic regulatory mechanisms of neurological disorders.

2023-08-21 | GSE236352 | GEO

The histone lysine demethylase KDM7A contributes to reward memory via Fscn1-induced synaptic plasticity in the medial prefrontal cortex

Project description:Lysine demethylase 7A (KDM7A) catalyzes the removal of dimethylation from histone H3 lysine 9 and lysine 27, both of which are associated with transcription repression. Previous study indicated that Kdm7a mRNA in the medial prefrontal cortex (mPFC) increased after drug exposure, yet its role in drug-related behaviors is largely unknown. In a morphine-conditioned place preference (CPP) paradigm, our findings revealed a specific increase of Kdm7a expression in the mPFC seven days after drug withdrawal. Subsequently, our results demonstrated that knockdown of Kdm7a in the mPFC did not affect the acquisition of morphine-induced CPP, but it attenuated memory consolidation. To further explore Kdm7a-mediated transcriptomic changes, we employed Nanopore direct RNA sequencing. Transcriptome profiling unveiled several gene expression alterations impacted by KDM7A, which were enriched in relevant neural function categories. Notably, we identified and validated fascin actin-bundling protein 1 (Fscn1) as a downstream molecular target. Knockdown of Fscn1 had a similar impact on CPP to Kdm7a, along with a corresponding decrease in dendritic spine density in the mPFC. Additionally, ChIP analysis demonstrated that silencing Kdm7a in N2a cells resulted in decreased enrichment of H3K9me2 and H3K27me2 at the Fscn1 promoter region, suggesting that Kdm7a may act as a crucial regulator of transcriptional responses to morphine-related reward memory via Fscn1.

2025-03-19 | GSE276730 | GEO

Transcriptome analysis of Kdm7a-deficient RAW264.7 cells during macrophage polarization.

Project description:Transcriptome analysis of Kdm7a-deficient RAW264.7 cells revealed that Kdm7a suppresses excessive polarization toward M2 macrophages.

2026-03-03 | GSE290919 | GEO

Inhibitors of the histone lysine demethylase KDM1A are broadly efficacious in AML by evicting the enzyme from chromatin [RNA-Seq]

Project description:Investigating the effects of two different classes of KDM1A inhibitors on the transcriptome of AML cell lines 16 different samples with biological replicates. Treatment for 24 and 72 hours with an irreversible KDM1A inhibitor (RN-1) or a reversible KDM1A inhibitor (GSK690) or an inactive isomer of the latter (GSK690*).

2016-02-10 | E-GEOD-71740 | biostudies-arrayexpress

Illumina Microarray of T47D cell with or without KDM7A-DT silencing under normal and oxidative stress conditions

Project description:KDM7A Divergent Transcript (KDM7A-DT) is a stress-induced lncRNAs. In our previous studies, KDM7A-DT showed the most robust cellular phenotype alteration and a significant TP53-dependency upon oxidative and oncogenic stress induction. Since about 50% of human breast cancers have mutant p53 and associated genetic alterations, it is essential to determine what effect a mutant p53 would have on acquired pro-oncogenic functions of KDM7A-DT. In these experiments, we used four antisense LNA Gapmer sequences designed by Exiqon (Vedbaek, Denmark). One of these was a negative control, while the other 3 were designed to target the end of the transcript representing the full-length lncRNA KDM7A-DT (lncRNA; GRCh38/hg38, chr7: 140,178,951-140,179,640). To test the effect of KDM7-DT in the context of mutant p53, we selected the p53-negative luminal BC cells T47D. For each of the LNA gapmers, we utilized 3 technical replicates across two main experimental conditions (normal vs. oxidative stress induced via 30 mins of 0.2 mM H2O2 treatment). Overall, we measured the signals for 47,323 Illumina array probes across 24 individual experiments (4 LNA gapmers * 3 technical replicates * 2 main experimental conditions).

2023-05-01 | E-MTAB-11818 | biostudies-arrayexpress

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