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Fragile X Syndrome causes epigenetic disruptions treatable with BET inhibitor Jq1

ABSTRACT: Fragile X Syndrome causes epigenetic disruptions treatable with BET inhibitor Jq1

PROVIDER: PRJNA323397 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR3583330.fastq.gz	Fastqsanger.gz
	SRR3583340.fastq.gz	Fastqsanger.gz
	SRR3588740.fastq.gz	Fastqsanger.gz
	SRR3588750.fastq.gz	Fastqsanger.gz
	SRR3583331.fastq.gz	Fastqsanger.gz

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Fragile X Syndrome causes epigenetic disruptions treatable with BET inhibitor Jq1

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

2017-08-18 | GSE81912 | GEO

Gene expression profiling of MYC-amplified medulloblastoma cell lines treated by JQ1, a BET bromodomain inhibitor

Project description:MYC-amplified medulloblastomas are highly lethal tumors. BET bromodomain inhibition was recently described to downregulate MYC-associated transcriptional activity in various cancer subtypes. To investigate whether JQ1, a BET bromodomain inhibitor is downregulation MYC and MYC-associated transcriptional activity, we performed global gene expression profiling of five medulloblastomas MYC-amplified patient-derived cell lines treated by JQ1 and the inactive form of JQ1. Five medulloblastomas patient-derived MYC-amplified cell lines were treated with the active and the inactive form of the drug (JQ1S or JQ1R, respectively, 1μM for 24 hours) followed by RNA extraction and hybridization on Affymetrix microarrays

2013-12-02 | E-GEOD-51020 | biostudies-arrayexpress

Gene expression profiling of MYC-amplified medulloblastoma cell lines treated by JQ1, a BET bromodomain inhibitor

2013-12-02 | GSE51020 | GEO

JQ1 promotes invasion in a BET protein independent manner in prostate cancer

Project description:Recent findings have shown that inhibitors targeting BET (bromodomain and extraterminal domain) proteins, such as the small molecule JQ1, are potent growth inhibitors of many cancers and hold promise for cancer therapy. However, some reports also have revealed that JQ1 can activate additional oncogenic pathways and may affect EMT (epithelial mesenchymal transition). Therefore, it is important to address the potential unexpected effect of JQ1 treatment, such as cell invasion and metastasis. Here, we showed that in prostate cancer, JQ1 inhibited cancer cell growth but promoted invasion and metastasis in a BET protein independent manner. Multiple invasion pathways including EMT, BMP (bone morphogenetic protein) signaling, chemokine signaling and focal adhesion pathway were activated by JQ1 to promote invasion. Notably, JQ1 induced upregulation of invasion genes through inhibition of FOXA1, an invasion suppressor in prostate cancer. JQ1 directly interacted with FOXA1, inactivated FOXA1 binding to its interacting repressors, TLE3, HDAC7 and NFIC, thus blocking FOXA1 repressive function and activating the invasion genes. Our finding indicates that JQ1 has an unexpected effect of promoting invasion in prostate cancer. Thus, the ill effect of JQ1 or its derived therapeutic agents could not be ignored during cancer treatment, especially in FOXA1 related cancers.

2022-10-01 | GSE139230 | GEO

Expression data from non-small cell lung cancer cell line DV90 after Bromodomain and extra terminal domain (BET) inhibitor JQ1 treatment

Project description:Bromodomain and extra terminal domain (BET) inhibition reduces occupancy of BET-family proteins at promoter and enhancer sites resulting in changes in the transcription of specific genes. We used microarray profiling to investigate the transcriptional changes induced by BET inhibitor JQ1 treatment in DV90 cells to identify the underlying changes of gene regulation that lead to JQ1 sensitivity. DV90 cells (JQ1 sensitive non-small cell lung cancer cell line) were treated with 135 nM (IC50) or 785 nM (IC90) of JQ1 for 4h and 24h. DMSO treated controls served as reference and at least four replicates per condition were collected. RNA was extracted and hybridized to Affymetrix HuGene-2.1ST microarrays to identify treatment induced transcriptional changes.

2016-03-31 | E-GEOD-75960 | biostudies-arrayexpress

Dose response of the BET inhibitor JQ1 in Small-Cell Lung Cancer cell lines.

Project description:This is a Dose response experiment carried out using the BET inhibitor JQ1 in SCLC cell lines. Approximately 1x106 cells of cell lines, DMS-53, H69, H1694, H1048, H2227 were treated for 2 hours with a 12 point dose range of JQ1 (7500nM to 0.04nM). Lysates were collected at the end of the treatment in 300ul TRI reagent for RNA preparation for expression profiling.

2015-05-31 | E-MTAB-3449 | biostudies-arrayexpress

RNA-seq analysis of SCC1 cells after JQ1, I-BET and/or INF-r treatment

Project description:In order to examine how BET inhibition affects the gene transcriptome in HNSCC cells, we performed RNA-sequencing in SCC1 cells treated with JQ1, I-BET, and/or INF-r.

2024-01-02 | GSE164155 | GEO

Human prostate cancer cell lines treated with BET Bromodomain inhibitor JQ1

Project description:RNA-Sequencing data for DU145 and PC3 cell lines treated with two concentrations of JQ1 in combination with IFN-y to determine effects of BET Bromodomain inhibition on prostate cancer cell lines

2019-02-20 | GSE126779 | GEO

BET Protein Inhibitor JQ1 Induces Cell Cycle Arrest in Mesenchymal Stem Cells

Project description:Efficacy and safety of anticancer drugs are traditionally studied using cancer cell lines and animal models. Recently, a potential anticancer agent, JQ1, an inhibitor of bromodomain and extra terminal (BET) protein, has been shown to promote apoptosis of cancerous cells by arresting them in G1 phase of the cell cycle. However, the effect of JQ1 on normal cells is poorly understood. In this study, we investigated the safety of JQ1 by using human umbilical cord mesenchymal stem cells (MSCs) as an in vitro model system. Our results indicated that JQ1 induced cell cycle arrest in G1 phase of MSCs, but did not promote apoptosis. Microarray analysis of MSCs treated with JQ1 indicated that it down-regulated genes involved not only in cell cycle regulation but also DNA replication, mitosis, and cell division. Although many studies have suggested the potential of JQ1 as an anticancer agent, our findings suggest that it caused a deleterious effect on normal cells and may not be safe for anticancer therapy. Human umbilical cord derived MSCs were cultured in vitro and treated with either 100 nM or 500 nM JQ1 for 24 hrs. Gene expression of treated cells was compared to untreated cultured cells.

2016-02-12 | E-GEOD-70577 | biostudies-arrayexpress

Effect of BET bromodomain inhibition with JQ1 in stressed human derived iPS cardiomyocytes

Project description:Gene expression profile of endothelin-1 (ET-1) stressed human derived iPS cardiomyocytes (from Cellular Dynamics) with or without the BET bromodomain inhibitor JQ1

2017-03-30 | GSE96560 | GEO

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