Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptional response to PORCN inhibition using an in vitro model of RNF43 mutant pancreatic adenocarcinoma (HPAF-II)

ABSTRACT: SRP136961 - PRJNA448457 - RNA-seq of response to PORCN inhibition, using ETC-159, in vitro of RNF43 mutant pancreatic adenocarcinoma (HPAF-II).

ORGANISM(S): Homo sapiens

PROVIDER: GSE118190 | GEO | 2018/12/04

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Transcriptional response to PORCN inhibition using an orthotopic model of RNF43 mutant pancreatic adenocarcinoma (HPAF-II)

Project description:Timecourse RNA-seq of response to PORCN inhibition, using ETC-159, in an orthotopic model of RNF43 mutant pancreatic adenocarcinoma (HPAF-II).

2018-12-04 | GSE118041 | GEO

Transcriptional response to PORCN inhibition using a subcutaneous model of RNF43 mutant pancreatic adenocarcinoma (HPAF-II)

Project description:SRP136970 - PRJNA448481 - RNA-seq of response to PORCN inhibition, using ETC-159,in a subcutanenous model of RNF43 mutant pancreatic adenocarcinoma (HPAF-II).

2018-12-04 | GSE118179 | GEO

Transcriptional response to PORCN inhibition using an in vivo model of RNF43 mutant pancreatic adenocarcinoma (HPAF-II) in EP300 knockout and WT cells

Project description:RNF43-mutant pancreatic tumors are driven by Wnt signaling and sensitive to Wnt inhibition, e.g. PORCN inhibitors. However, some RNF43-mutant pancreatic cancers are intrinsically resistant to Wnt inhibition. We identified that EP300 mutations confer resistance to PORCN inhibitors in RNF43-mutant pancreatic cancers. We found that EP300 knockout down-regulated GATA6 expression and GATA6-regulated differentiation program, making the anti-differentiation roles of Wnt signaling dispensable.

2022-06-16 | GSE183893 | GEO

Transcriptional response to PORCN inhibition using an HPAF-II orthotopic model upon MYC perturbation

Project description:SRP137043 - PRJNA448654 - Timecourse RNA-seq response to PORCN inhibition using an HPAF-II orthotopic model with different MYC states

2018-12-04 | GSE118231 | GEO

Wnt addiction of genetically defined cancers reversed by PORCN inhibition

Project description:Enhanced sensitivity to Wnts is an emerging hallmark of a subset of cancers, defined in part by mutations regulating the abundance of their receptors. Inhibition of Wnt secretion by blocking an essential post-translational modification, palmitoleation, provides a useful therapeutic intervention. Inhibition of PORCN in RSPO3-translocated cancers via treatment with ETC-159 causes a marked remodeling of the transcriptome, with loss of cell cycle, stem cell, and proliferation genes and an increase in differentiation markers. Inhibition of Wnt signaling by PORCN inhibition holds promise as differentiation therapy in genetically defined human cancers. RNA-seq of colorectal PDXs with confirmed R-spondin fusion genes. RNA-seq was performed in 2 conditions (Vehicle and treatment with ETC-159 (an inhibitor of PORCN) with 4 replicates per condition.

2015-08-12 | E-GEOD-69687 | biostudies-arrayexpress

Wnt addiction of genetically defined cancers reversed by PORCN inhibition

2015-08-12 | GSE69687 | GEO

Transcriptional response to PORCN inhibition using an in vivo model of RNF43 mutant pancreatic adenocarcinoma (HPAF-II) in EP300 knockout and WT cells

Project description:Transcriptional response to PORCN inhibition using an in vivo model of RNF43 mutant pancreatic adenocarcinoma (HPAF-II) in EP300 knockout and WT cells

| PRJNA762294 | ENA

Expression data from HepG2 cells before and after RNF43 knockdown

Project description:It has been demonstrated that Ring finger protein 43 (RNF43) is overexpressed in colorectal cancer and mediates cancer cell proliferation. We found that RNF43 was frequently overexpressed in HCC, and knockdown of RNF43 could induce apoptosis and inhibit proliferation, invasion, colony formation and xenograft growth of HCC cells. Suggesting that RNF43 is involved in tumorigenesis and progression of HCC. We used microarrays to profile gene expression patterns before and after RNF43 knockdown, and identified differentially expressed genes during this process. HepG2 cells were transfected with RNF43 siRNA or negative control siRNA in triplicate. Forty-eight hours after transfection, total RNA was extracted,labeled and hybridized to HG-U133 Plus 2.0 arrays.

2012-10-04 | E-GEOD-41326 | biostudies-arrayexpress

Expression data from HepG2 cells before and after RNF43 knockdown

2012-10-04 | GSE41326 | GEO

RNF43 truncations trap CK1 to drive niche-independent self-renewal in cancer

Project description:Wnt/b-catenin signaling is a primary pathway for stem cell maintenance during tissue renewal and a frequent target for mutations in cancer. Impaired Wnt receptor endocytosis due to loss of the ubiquitin ligase RNF43 gives rise to Wnt-hypersensitive tumors that are susceptible to anti-Wnt-based therapy. Contrary to this paradigm, we identify a class of RNF43 truncating cancer mutations that induce b-catenin-mediated transcription, despite exhibiting retained Wnt receptor downregulation. These mutations interfere with an ubiquitin-independent suppressor role of the RNF43 cytosolic tail that involves casein kinase-1 (CK1) binding and phosphorylation. Mechanistically, truncated RNF43 variants trap CK1 at the plasma membrane, thereby preventing b-catenin turnover and propelling ligandindependent target gene transcription. Gene editing of human colon stem cells shows that RNF43 truncations cooperate with p53 loss to drive a niche-independent program for self-renewal and proliferation. Moreover, these RNF43 variants confer decreased sensitivity to anti-Wnt-based therapy. Our data demonstrate the relevance of studying patient-derived mutations for understanding disease mechanisms and improved applications of precision medicine.

2020-08-14 | PXD020478 | Pride

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