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Effects of BRD4 inhibitor JQ1 on the expression profile in cervical cancer HeLa cells

ABSTRACT: Effects of BRD4 inhibitor JQ1 on the expression profile in cervical cancer HeLa cells

PROVIDER: PRJNA984216 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24928370_1.fastq.gz	Fastqsanger.gz
	SRR24928370_2.fastq.gz	Fastqsanger.gz
	SRR24928371_1.fastq.gz	Fastqsanger.gz
	SRR24928371_2.fastq.gz	Fastqsanger.gz
	SRR24928372_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Effects of BRD4 inhibitor JQ1 on the expression profile in cervical cancer HeLa cells

Project description:The potential antitumor effects of JQ1 on cervical cancer cells and its impact on the expression profile remain unknown. To explore the mechanism of JQ1 affecting the progression of cervical cancer, this study used high-throughput sequencing technology to investigate the transcriptome changes of cervical cancer cells treated with JQ1 to reveal the signal pathway and biological function of JQ1 on cervical cancer cells and to provide transcriptome evidence for the application of cervical in the potential treatment of cervical cancer.

2024-02-09 | GSE235031 | GEO

Transcriptome analysis of dominant-negative Brd4 mutants identifies Brd4-specific target genes of BET inhibitor JQ1

Project description:We analyzed anti-proliferative dominant-negative Brd4 mutants that compete with the function of distinct Brd4 domains. We used these Brd4 mutants to compare the Brd4-specific transcriptome with the transcriptome of JQ1 treated cells.

2017-06-09 | GSE92456 | GEO

IDR-Targeting Compounds Suppress HPV Genome Replication via Disruption of Phospho-BRD4 Association with DNA Damage Response Factors

Project description:Perturbation of genome-wide expression profiles and BRD4 isoform (BRD4-L and BRD4-S) binding by phospho-BRD4-targeting compounds (pNPS14, pNPS90, or pNPS145) or BET bromodomain inhibitor JQ1 in proliferating and differentiated W12E human cervical keratinocytes

2023-12-15 | GSE228786 | GEO

An atheroprotective transcriptome induced by JQ1 (a BRD4 inhibitor) in human endothelial cells

Project description:The bromodomain and extra terminal domain (BET) family of proteins, including BRD2, BRD3, and BRD4, play a key role in many cellular processes, including inflammatory gene expression, mitosis, and viral/host interaction by controlling the assembly of histone acetylation-dependent chromatin complexes. Previous studies have shown that multiple BET inhibitors (BETi), including JQ1, have therapeutic effects in cancer and cardiovascular diseases. Some BETi have entered different phases of clinical trials. Pharmacologically, JQ1 functions by displacing BET proteins from chromatin by competitively binding to the acetyl-lysine recognition pocket of BET bromodomains. JQ1 has been used as a chemical probe to investigate the role of BET bromodomains in the transcriptional regulation of cardiovascular diseases. For example, JQ1 has been shown to attenuates inflammation and experimental atherosclerosis (Mol Cell. 2014 Oct 23; 56(2): 219–231.). JQ1 has also recently been shown to reduce EndoMT and cardiac fibrosis (J Mol Cell Cardiol. 2019 Feb;127:83-96.). However, the molecular targets of JQ1 dependent or independent of BRD4 remains unknown. To depict the transcriptomic signature of JQ1 in human endothelial cells, we observed a vasoprotective and atheroprotective transcriptome by JQ1 treatment using genome-wide RNA-seq based transcriptomic profiling. JQ1 is a magic bullet in cardiovascular disease prevention. Further elucidation of new molecular targets of JQ1 will lead to the identification of potentially new therapeutic targets to treat cardiovascular diseases.

2019-11-27 | GSE137500 | GEO

BRD4 inhibitor JQ1 increase the sensitivity of arsenic trioxide in pancreatic cancer

Project description:BRD4 inhibitor JQ1 increase the sensitivity of arsenic trioxide in pancreatic cancer

| PRJNA510651 | ENA

Effects of BRD4 inhibition in AML

Project description:The BET (bromodomain and extra terminal) protein family members including BRD4 bind to acetylated lysines on histones and regulate the expression of important oncogenes, e.g., MYC and BCL2. Here we demonstrate the sensitizing effects of the histone hyperacetylation inducing pan-histone deacetylase inhibitor (HDI) panobinostat (PS) on human AML blast progenitor cells (BPCs) to the BET protein inhibitor JQ1. Treatment with JQ1 but not its inactive enantiomer (R-JQ1) was highly lethal against AML BPCs expressing mutant NPM1c+ with or without co-expression of FLT3-ITD, or AML expressing MLL fusion oncoprotein. JQ1 treatment reduced binding of BRD4 and RNA polymerase II to the DNA of MYC and BCL2, and reduced their levels in the AML cells. Co-treatment with JQ1 and the HDAC inhibitor panobinostat (PS) synergistically induced apoptosis of the AML BPCs, but not of normal CD34+ hematopoietic progenitor cells. This was associated with greater attenuation of MYC and BCL2, while increasing p21, BIM and cleaved PARP levels in the AML BPCs. Co-treatment with JQ1 and PS significantly improved the survival of the NOD/SCID mice engrafted with OCI-AML3 or MOLM13 cells (p < 0.01). These findings highlight co-treatment with a BRD4 antagonist and an HDI as a potentially efficacious therapy of AML. Two samples were analyzed (untreated cells, cells treated with JQ1)

2014-01-01 | E-GEOD-51950 | biostudies-arrayexpress

An atheroprotective transcriptome induced by JQ1 (a BRD4 inhibitor) in human endothelial cells

Project description:An atheroprotective transcriptome induced by JQ1 (a BRD4 inhibitor) in human endothelial cells

| PRJNA565731 | ENA

ChIP-seq analysis of BRD4, MED1 and P65 in SCC1 cells after JQ1 treatment

Project description:To explore genome-wide alteration of BRD4, MED1, p65 and H3K27Ac during BET inhibition, we performed chromatin immunoprecipitation sequencing (ChIP-seq) of SCC1 cells to examine genome-wide recruitment of the MED1, BRD4, p65 and H3K27ac following JQ1 treatment. BET inhibition by JQ1 led to dramatically loss of the recruitment of MED1, BRD4 and p65 at a cohort of key oncogenes associate with tumorigenesis and metastasis. Suggesting BET inhibition is effective strategy to suppress the tumorigenesis and metastasis of head and neck squamous cell carcinoma.

2021-05-05 | GSE131710 | GEO

Small-molecule inhibitor JQ1 effect on multiple myeloma cell lines

Project description:Pathologic activation of c-Myc plays a central role in pathogenesis of several neoplasias, including multiple myeloma. However, therapeutic targeting of c-Myc has remained elusive due to its lack of a clear ligand-binding domain. We therefore targeted c-Myc transcriptional function by another means, namely the disruption of chromatin-dependent signal transduction. Members of the bromodomain and extra-terminal (BET) subfamily of human bromodomain proteins (BRD2, BRD3 and BRD4) associate with acetylated chromatin and facilitate transcriptional activation by increasing the effective molarity of recruited transcriptional activators. Notably, BRD4 marks select M/G1 genes in mitotic chromatin for transcriptional memory and direct post-mitotic transcription, via direct interaction with the positive transcription elongation factor complex b (P-TEFb). Because c-Myc is known to regulate promoter-proximal pause release of Pol II, also through the recruitment of P-TEFb, we evaluated the selective small-molecule inhibitor of BET bromodomains, JQ1, as a chemical probe to interrogate the role of BET bromodomains in Myc-dependent transcription and to explore their role as therapeutic targets in c-Myc-driven neoplasias. Duplicate cultures of MM.1S, OPM1 and KMS11 human myeloma cells were treated with either DMSO alone or with JQ1 (500 nM), for 24 hours. Total RNA was extracted and hybridized to Affymetrix human Gene 1.0 ST microarrays (two arrays per treatment per cell line for a total of 12 arrays).

2011-09-01 | E-GEOD-31365 | biostudies-arrayexpress

BRD4 represses CBX5

Project description:BRD4 is amplified and/or up-regiulated in a subset of ovarian cancer which correlates with a poor survival siRNA sensitization screens in the presence of CHK1 inhibitor, LY2606368, identify BRD4 as a therapeutic target in ovarian cancer. BRD4 suppression by either siRNA or using JQ1 increases CBX5 expression

2016-05-01 | GSE78704 | GEO

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