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ZBTB7A is a modulator of KDM5-driven transcriptional networks in basal breast cancer (ChIP-Seq)

ABSTRACT: ZBTB7A is a modulator of KDM5-driven transcriptional networks in basal breast cancer (ChIP-Seq)

PROVIDER: PRJNA1080532 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28094219_1.fastq.gz	Fastqsanger.gz
	SRR28094219_2.fastq.gz	Fastqsanger.gz
	SRR28094220_1.fastq.gz	Fastqsanger.gz
	SRR28094220_2.fastq.gz	Fastqsanger.gz
	SRR28094221_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

ZBTB7A is a modulator of KDM5-driven transcriptional networks in basal breast cancer (RNA-Seq)

Project description:We previously identified KDM5B, encoding a histone H3 lysine 4 (H3K4) demethylase, as an oncogene in estrogen receptor positive (ER+) breast cancer driving endocrine resistance. Here we describe that KDM5A is frequently amplified and overexpressed in basal breast tumors and is associated with chemotherapy resistance. Using CRISPR knockout viability screens -/+ KDM5 inhibition (KDM5i), we found that deletion of the transcription factor ZBTB7A and core SAGA complex increased sensitivity to KDM5i, whereas knockout of RHO-GTPases led to resistance. Integrated ChIP-seq and RNA-seq analyses revealed colocalization of ZBTB7A and KDM5s at promoters with high H3K4me3 signal and dependence of KDM5A binding on ZBTB7A. ZBTB7A knockout had a pleiotropic effect on transcriptional responses to KDM5i, in which it modulates the KDM5i-induced innate immune signaling and NF-kB-regulated genes. ZBTB7A knockout and KDM5i cooperate to alter cell states with KDM5i decreasing basal-like and ZBTB7A knockout inducing mesenchymal-like gene expression patterns. Our work furthers our understanding of KDM5-mediated gene regulation in breast cancer and identifies key pathways that mediate sensitivity to KDM5 inhibition

2024-10-14 | GSE259249 | GEO

ZBTB7A is a modulator of KDM5-driven transcriptional networks in basal breast cancer (ChIP-Seq)

2024-10-14 | GSE259248 | GEO

ZBTB7A is a modulator of KDM5-driven transcriptional networks in basal breast cancer

Project description:ZBTB7A is a modulator of KDM5-driven transcriptional networks in basal breast cancer

| PRJNA1080529 | ENA

ZBTB7A is a modulator of KDM5-driven transcriptional networks in basal breast cancer (scRNA-seq)

Project description:ZBTB7A is a modulator of KDM5-driven transcriptional networks in basal breast cancer (scRNA-seq)

| PRJNA1095998 | ENA

ZBTB7A is a modulator of KDM5-driven transcriptional networks in basal breast cancer (RNA-Seq)

Project description:ZBTB7A is a modulator of KDM5-driven transcriptional networks in basal breast cancer (RNA-Seq)

| PRJNA1080531 | ENA

ZBTB7A is a modulator of KDM5-driven transcriptional networks in basal breast cancer (scRNA-seq)

2024-10-14 | GSE263161 | GEO

ZBTB7A and KDM5 activity co-regulate NF-kB target gene expression and oxidative phosphorylation in triple negative breast cancer

Project description:We previously described that the KDM5B histone H3 lysine 4 (H3K4) demethylase is an oncogene in estrogen receptor-positive breast cancer. Here we report that KDM5A is amplified and overexpressed in basal breast tumors and is associated with chemotherapy resistance. Using CRISPR knockout viability screens -/+ KDM5 inhibition (KDM5i), we found that deletion of the ZBTB7A transcription factor and core SAGA complex sensitized to KDM5i, whereas knockout of RHO-GTPases led to resistance. ChIP-seq and RNA-seq analyses revealed colocalization of ZBTB7A and KDM5A/B at promoters with high H3K4me3 and dependence of KDM5A binding on ZBTB7A. ZBTB7A knockout altered transcriptional response to KDM5i specifically at NF-kB target genes, oxidative phosphorylation, and E2F-driven proliferation pathways. Our work furthers understanding of KDM5-mediated gene regulation in breast cancer and identified key pathways mediating sensitivity to KDM5i.

2024-04-02 | MSV000094452 | MassIVE

ZBTB7A is a modulator of KDM5-driven transcriptional networks in basal breast cancer

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

2024-10-14 | GSE259252 | GEO

Genome-wide maps of KDM5 binding in drosophila adults

Project description:To determine which genes affected by loss of KDM5 in adults were direct targets, we carried out KDM5 ChIP-seq analyses. To valide this data, we utilized a previously generated fly strain in which the sole source of KDM5 is from a transgene expressing an HA tagged form of KDM5 expressed under the control of its endogenous promoter. Comparing genome-wide gene expression and KDM5 binding analyses in Drosophila adults, we demonstrate the primary function of KDM5 in adults is to activate gene expression KDM5. To investigate the link between KDM5 and H3K4me3, we carried out anti-H3K4me3 ChIP-seq from wildtype adults . Genome-wide, KDM5 and H3K4me3 peaks showed a similar distribution, with both peaking at the transcription start site (TSS) showed a striking overlap with the presence of H3K4me3. Examination of KDM5 binding and histone H3K4me3 modifications in drosophila adults

2015-12-22 | E-GEOD-70589 | biostudies-arrayexpress

ZBTB7A ChIP-seq under different DHT level

Project description:Zinc finger and BTB domain containing transcription repressor ZBTB7A has been recently reported as a tumor suppressor who plays important functions to prevent the progression of prostate cancer. However, the chromatin activity of ZBTB7A in prostate cancer cells remain unclear. In order to identify the cistrome and transcriptome of ZBTB7A, we performed ZBTB7A ChIP-seq in VCaP cells and RNA-seq in VCaP cells transfected with siRNA targeting ZBTB7A or non-targeting control, respectively (cells were grown in full serum). By using combined ChIP-seq and RNA-seq analyses in VCaP cells, we have precisely mapped the ZBTB7A binding sites and identified a subset of genes that are directly repressed by ZBTB7A. To study the chromatin interaction of ZBTB7A with androgen receptor (AR), we also performed ChIP-seq of ZBTB7A in VCaP cells stimulated with 10 nM DHT for 4 hours versus vehicle control (cells were hormone-depleted prior to DHT stimulation). Our results show that ZBTB7A binding is increased by androgen at AR and ZBTB7A overlapping sites.

2019-09-12 | GSE123089 | GEO

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