Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

PROTEIN KINASE C EPSILON COOPERATES WITH PTEN LOSS FOR PROSTATE TUMORIGENESIS THROUGH THE CXCL13-CXCR5 PATHWAY

ABSTRACT: PKCe, an oncogenic member of the PKC family, is aberrantly overexpressed in epithelial cancers. To date, little is known about functional interactions of PKCe with other genetic alterations and the effectors of this kinase that contribute to its tumorigenic and metastatic phenotype. Here we demonstrate that PKCe cooperates with the loss of the tumor suppressor Pten for the development of prostate cancer in a mouse model. Mechanistic analysis revealed that PKCe overexpression and Pten loss individually and synergically cause a remarkable up-regulation in the production of the chemokine CXCL13. Notably, targeted disruption of CXCL13 or its receptor CXCR5 in prostate cancer cells impaired their migratory and tumorigenic properties. In addition to providing evidence for an autonomous vicious cycle driven by PKCe, our studies identified a compelling rationale for targeting the CXCL13:CXCR5 axis for prostate cancer treatment.

ORGANISM(S): Mus musculus

PROVIDER: GSE86257 | GEO | 2017/04/01

SECONDARY ACCESSION(S): PRJNA341321

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

The healing myocardium mobilizes a distinct B-cell subset through a CXCL13-CXCR5-dependent mechanism

Project description:Recent studies have revealed that B-cells can influence post-myocardial infarction (MI) inflammation and repair, but the mechanisms controlling their mobilization and in situ activity remain poorly understood. Herein, we sought to dissect the mechanisms underlying B-cell cardiotropism and assess the B-cell antigen specificity profile in an experimental model of MI. Our study reveals that B-cells that are not antigen-specifically expanded readily infiltrate the infarcted myocardium via the CXCL13-CXCR5 axis. The restricted distribution of CXCR5 among hB cells could offer a suitable opportunity to selectively target this leukocyte subset therapeutically while minimally interfering with other local or systemic immunological processes.

2021-05-29 | GSE150140 | GEO

Disturbed glycolipid metabolism activates CXCL13-CXCR5 axis in senescent TSCs to promote heterotopic ossification formation

Project description:Heterotopic ossification (HO) occurs as a common complication after injury, while its risk factor and mechanism remain unclear yet, which restricts the development of pharmacological treatment. Clinical research suggested that diabetes mellitus (DM) patients were prone to develop HO in tendon, but the solid evidence and mechanical research are still needed. Here, we combined the clinical samples and DM mice model to identify that disordered glycolipid metabolism aggravates the senescence of tendon derived stem cells (TSCs) and promotes their osteogenic differentiation. Then, combining the RNA-seq results of aging tendon, we detected the abnormally activated autocrine CXCL13-CXCR5 axis in TSCs cultured in high fat high glucose (HFHG) environment and also in aged tendon. Genetic inhibition of CXCL13 successfully alleviates the HO formation in DM mice, providing a potential therapeutical target for suppressing HO formation in DM patients after trauma or surgery.

2024-08-28 | GSE234916 | GEO

Lack of chemokine signaling through CXCR5 causes mortality, ventricular dilatation and deranged matrix during pressure overload

Project description:Inflammatory mechanisms have been suggested to play a role in the development of heart failure (HF), but a role for chemokines is largely unknown. The aim of this study was to analyze the role of the chemokine CXCL13 and its receptor CXCR5 in cardiac pathophysiology leading to HF A microarray study was performed on seven mice harboring a systemic knockout of the CXCR5 (CXCR5-/-) and seven wildtype mice. Four of the knockouts and four of the wild type mice were subjected to aorta banding and three of each to sham operations.

2010-10-01 | E-GEOD-22295 | biostudies-arrayexpress

The healing myocardium mobilizes a distinct B-cell subset through a CXCL13-CXCR5-dependent mechanism

Project description:The healing myocardium mobilizes a distinct B-cell subset through a CXCL13-CXCR5-dependent mechanism

| PRJNA631246 | ENA

Disturbed glycolipid metabolism activates CXCL13-CXCR5 axis in senescent TSCs to promote heterotopic ossification formation

Project description:Disturbed glycolipid metabolism activates CXCL13-CXCR5 axis in senescent TSCs to promote heterotopic ossification formation

| PRJNA983738 | ENA

Lack of chemokine signaling through CXCR5 causes mortality, ventricular dilatation and deranged matrix during pressure overload

2010-10-01 | GSE22295 | GEO

Protein Kinase C Epsilon Cooperates with PTEN Loss for Prostate Tumorigenesis through the CXCL13-CXCR5 Pathway.

Project description:PKCε, an oncogenic member of the PKC family, is aberrantly overexpressed in epithelial cancers. To date, little is known about functional interactions of PKCε with other genetic alterations, as well as the effectors contributing to its tumorigenic and metastatic phenotype. Here, we demonstrate that PKCε cooperates with the loss of the tumor suppressor Pten for the development of prostate cancer in a mouse model. Mechanistic analysis revealed that PKCε overexpression and Pten loss individually and synergistically upregulate the production of the chemokine CXCL13, which involves the transcriptional activation of the CXCL13 gene via the non-canonical nuclear factor κB (NF-κB) pathway. Notably, targeted disruption of CXCL13 or its receptor, CXCR5, in prostate cancer cells impaired their migratory and tumorigenic properties. In addition to providing evidence for an autonomous vicious cycle driven by PKCε, our studies identified a compelling rationale for targeting the CXCL13-CXCR5 axis for prostate cancer treatment.

| S-EPMC5444089 | biostudies-literature

The age of the bone marrow microenvironment influences B-cell acute lymphoblastic leukemia progression via CXCR5-CXCL13

Project description:The age of the bone marrow microenvironment influences B-cell acute lymphoblastic leukemia progression via CXCR5-CXCL13

| PRJNA755248 | ENA

Mus musculus

Project description:PROTEIN KINASE C EPSILON COOPERATES WITH PTEN LOSS FOR PROSTATE TUMORIGENESIS THROUGH THE CXCL13-CXCR5 PATHWAY

| PRJNA341321 | ENA

The age of the bone marrow microenvironment influences B-cell acute lymphoblastic leukemia progression via CXCR5-CXCL13 [ATAC-Seq]

Project description:The age of the bone marrow microenvironment influences B-cell acute lymphoblastic leukemia progression via CXCR5-CXCL13 [ATAC-Seq]

| PRJNA755258 | ENA

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