Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RB-N phosphorylation promotes BRD4-mediated CREB signaling hyperactivation and BET inhibitor resistance

ABSTRACT: The combination of CREB inhibitor and JQ1 could overcome the resistance to BET inhibitors in RB loss prostate cancer. Our study firstly showed that GNB1L-CREB pathway was activated after RB loss and considered as the potential target for the prostate cancer therapy

ORGANISM(S): Homo sapiens

PROVIDER: GSE191263 | GEO | 2022/08/30

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

RB-N phosphorylation promotes BRD4-mediated GPCR signaling hyperactivation and BET inhibitor resistance

Project description:The combination of CREB inhibitor and JQ1 could overcome the resistance to BET inhibitors in RB loss prostate cancer. Our study firstly showed that ADRB2-CREB pathway was activated after RB loss and considered as the potential target for the prostate cancer therapy

2021-12-31 | GSE162897 | GEO

RB-N phosphorylation promotes BRD4-mediated CREB signaling hyperactivation and BET inhibitor resistance

Project description:RB-N phosphorylation promotes BRD4-mediated CREB signaling hyperactivation and BET inhibitor resistance

| PRJNA790814 | ENA

RB-N phosphorylation promotes BRD4-mediated GPCR signaling hyperactivation and BET inhibitor resistance

Project description:RB-N phosphorylation promotes BRD4-mediated GPCR signaling hyperactivation and BET inhibitor resistance

| PRJNA683660 | ENA

Development of gene sets after deleting Rb in p53 null background primary prostate cells [Rb only]

Project description:Our findings suggested that cytokines were upregulated in p53 null primary prostate cells after deleting Rb. Rb deletion is important for prostate cancer progression.

2015-12-31 | GSE68903 | GEO

Development of gene sets after deleting Rb in p53 null background primary prostate cells [Rb only]

Project description:Our findings suggested that cytokines were upregulated in p53 null primary prostate cells after deleting Rb. Rb deletion is important for prostate cancer progression. p53-/- Rbf/f vs p53-/- Rbâf/âf primary prostate cells.Three independent experiments were performed.

2015-12-31 | E-GEOD-68903 | biostudies-arrayexpress

Development of gene sets after deleting Rb and Pten in p53 null background primary prostate cells [Rb and Pten]

2015-12-31 | GSE68904 | GEO

Development of gene sets after deleting Rb and Pten in p53 null background primary prostate cells [Rb and Pten]

Project description:Our findings suggested that cytokines were upregulated in p53 null primary prostate cells after deleting Rb and/or Pten. Rb and Pten deletion are important for prostate cancer progression. p53-/- Rbf/f vs p53-/- Rbâf/âf primary prostate cells. Three independent experiments were performed. p53-/- Rbf/f vs p53-/- Rbâf/âf Ptenâf/âf primary prostate cells. Four independent experiments were performed.

2015-12-31 | E-GEOD-68904 | biostudies-arrayexpress

Wild-type vs. Rb-/- Prostate Epithelial Cell Lines

Project description:Comparison of control wild-type and Rb-/- prostate epithelial cell lines under untreated and serum-free conditions Keywords = prostate Keywords = epithelial Keywords: other

2004-01-05 | GSE934 | GEO

Analyzing CREB binding motif and sites in the mouse lens epithelial cells alpha-TN4 overexpressing Vector, WT-CREB, S133A-CREB, R314A-CREB and S133A/R314A –CREB.

Project description:Transcription factor CREB regulates lens Epithelial-Mesenchymal Transition（EMT）in both S133 phosphorylation dependent and independent manners. We found that S133A-CREB can activate lens EMT, while R314A-CREB attenuated it. To understand the mechanism by which S133A-CREB and R314A-CREB modulates EMT gene expression. ChIP assay using CREB antibody in the in the mouse lens epithelial cells alpha-TN4 overexpressing Vector, WT-CREB, S133A-CREB, R314A-CREB and S133A/R314A-CREB, and ChIP-seq was conducted on the ChIP DNA. We found that WT-CREB, S133A-CREB as well as R314A-CREB binds to the promoter regions of mesenchymal genes, and S133A-CREB retained canonical CREB binding motif, while R314A-CREB exhibited shifted binding motif preference to ATF1.

2025-02-05 | GSE276462 | 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

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data