Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

DNA-dependent protein kinase drives prostate cancer progression through transcriptional regulation of the Wnt signaling pathway

ABSTRACT: DNA-dependent protein kinase drives prostate cancer progression through transcriptional regulation of the Wnt signaling pathway

PROVIDER: PRJNA480511 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

DNA-dependent protein kinase drives prostate cancer progression through transcriptional regulation of the Wnt signaling pathway

Project description:DNAPK was identified as the most significantly expressed kinase associated with metastatic progression in high-risk prostate cancer. GSEA analysis on DNAPK knockdwon samples and on patient data nominated Wnt signaling as the top pathway associated with DNAPK Our data indicates that DNAPK regulates Wnt signaling pathway.

2019-10-01 | GSE116895 | GEO

SOX9 Drives WNT Pathway Activation in Prostate Cancer

Project description:SOX9 Drives WNT Pathway Activation in Prostate Cancer

| PRJNA307342 | ENA

Epithelial Wnt secretion drives the progression of inflammation-induced colon carcinoma

Project description:Epithelial Wnt secretion drives the progression of inflammation-induced colon carcinoma

| PRJNA753131 | ENA

DNA-Dependent Protein Kinase Drives Prostate Cancer Progression through Transcriptional Regulation of the Wnt Signaling Pathway.

Project description: Not available

| S-EPMC6744969 | biostudies-literature

Wnt activator FOXB2 drives the neuroendocrine differentiation of prostate cancer

Project description:The Wnt signaling pathway is playing a crucial role during development and adult tissue homeostasis. However, the tissue and cell type-specific regulation of Wnt pathway activity remains incompletely understood. Here we identify FOXB2, an uncharacterized forkhead box family transcription factor, as a potent activator of Wnt signaling in normal and cancer cells. Proximity-dependent biotinylation assay (BioID) coupled with mass spectrometry identified transcriptional co-regulators required for FOXB2-dependent Wnt activation.

2019-10-16 | PXD015725 | Pride

SOX9 drives WNT pathway activation in prostate cancer.

Project description: Not available

| S-EPMC4855922 | biostudies-literature

The tumor suppressor kinase DAPK3 drives tumor-intrinsic immunity through the STING-IFNb pathway Phospho

Project description:Phosphoproteomics show that the tumor suppressor kinase DAPK3 drives tumor-intrinsic immunity through the STING-IFNb pathway

2021-01-15 | MSV000086706 | MassIVE

The tumor suppressor kinase DAPK3 drives tumor-intrinsic immunity through the STING-IFNb pathway Proteome

Project description:Proteome analysis reveals that the tumor suppressor kinase DAPK3 drives tumor-intrinsic immunity through the STING-IFNb pathway Proteome

2021-01-15 | MSV000086708 | MassIVE

Protein proximity networks and functional evaluation of the Casein Kinase 1 γ family reveals unique roles for CK1γ3 in WNT signaling

Project description:The WNT/β-catenin signaling pathway is evolutionarily conserved and controls normal embryonic development, adult tissue homeostasis, and regeneration. Aberrant activation or suppression of WNT signaling contributes to cancer initiation and progression, developmental disorders, neurodegeneration, and bone disease. Despite great need and more than 40 years of research, targeted therapies for the WNT pathway have yet to be fully realized. Kinases are exceptionally druggable and occupy key nodes within the WNT signaling network, but several pathway-relevant kinases remain understudied and ‘dark’. Here we studied the function of the CSNK1g subfamily of human kinases. miniTurbo-based proximity biotinylation and mass spectrometry analysis of CSNK1γ1, CSNK1γ2, and CSNK1γ3 revealed numerous established components of the β-catenin-dependent and independent WNT signaling pathways, as well as novel interactors. In gain-of-function experiments using a panel of transcriptional reporters, CSNK1γ3 but not CSNK1γ1 or CSNK1γ2 activated β-catenin-dependent WNT signaling, with minimal effect on other signaling pathways. Within the family, CSNK1γ3 expression uniquely induced LRP6 phosphorylation. Conversely, siRNA-mediated silencing of CSNK1γ3 alone had no impact on WNT signaling, though co-silencing of all three family members decreased WNT pathway activity. We characterized two moderately selective and potent small molecule inhibitors of the CSNK1γ family. These inhibitors and a CSNK1γ3 kinase dead mutant suppressed but did not eliminate WNT-driven LRP6 phosphorylation and β-catenin stabilization. Our data suggest that while CSNK1γ3 expression uniquely drives pathway activity, potential functional redundancy within the family necessitates loss of all three family members to suppress the WNT signaling pathway.

2022-06-09 | PXD032138 | Pride

PLEKHS1 drives PI3Ks and remodels pathway homeostasis in PTEN-null prostate

Project description:The PIP3/PI3K network is a central regulator of metabolism and is frequently activated in cancer, commonly by loss of the PIP3/PI(3,4)P2-phosphatase, PTEN. Despite huge investment, the drivers of the PI3K network in normal tissues and how they adapt to overactivation are unclear. We find that in healthy mouse prostate PI3K activity is driven by RTK/IRS signalling and constrained by pathway-feedback. In the absence of PTEN, the network is dramatically remodelled. A poorly understood, YXXM- and PIP3/PI(3,4)P2-binding PH domain-containing, adaptor, PLEKHS1, became the dominant activator and was required to sustain PIP3, AKT-phosphorylation and growth in PTEN-null prostate. This was because PLEKHS1 evaded pathway-feedback and experienced enhanced PI3K- and SRC-family kinase-dependent phosphorylation of Y258XXM, eliciting PI3K-activation. hPLEKHS1-mRNA and activating-Y419-phosphorylation of hSRC correlated with PI3K-pathway activity in human prostate cancers. We propose that in PTEN-null cells, receptor-independent, SRC-dependent tyrosine-phosphorylation of PLEKHS1 creates positive-feedback that escapes homeostasis, drives PIP3-signalling and supports tumour progression.

2023-08-23 | PXD043239 | Pride

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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