Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Identification of Wnt target genes associated with malignant phenotypes in CTNNB1-mutated NSCLC

ABSTRACT: Microarray analysis comparing the expression profiles of siRNA-mediated CTNNB1-silenced and CTNNB1-retained HCC15 cells harboring a homozygous CTNNB1 S45F mutation revealed that besides several known Wnt genes, LGR6 was significantly downregulated by CTNNB1 knockdown in HCC15 cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE183178 | GEO | 2022/09/01

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Identification of LGR6-associated genes in NSCLC

Project description:mRNA seq analysis comparing the expression profiles of siRNA-mediated LGR6-silenced and LGR6-retained NSCLC cell lines harboring CTNNB1 exon 3 mutations identified several LGR6-related genes that have been associated with cancer development and stemness properties.

2023-11-01 | GSE218163 | GEO

Identification of genes that confer cancer stem cell properties in CTNNB1-mutated NSCLC cells.

Project description:mRNA seq analysis comparing the expression profiles of sphere-forming and adherent A427 cells carrying a homozygous CTNNB1 T41A mutation revealed that several stem cell-associated genes and pathways were upregulated in the spheroid cultures.

2023-11-01 | GSE218164 | GEO

Seminiferous tubule degeneration and infertility in mice with sustained activation of WNT/CTNNB1 signaling in sertoli cells

Project description:To elucidate the role(s) of WNT/CTNNB1 signaling in the testis, transgenic Ctnnb1 tm1Mmt/+;Amhr2 tm3(cre)Bhr/+ mice were generated to obtain sustained activation of the WNT/CTNNB1 pathway in Sertoli cells. Male Ctnnb1 tm1Mmt/+;Amhr2 tm3(cre)Bhr/+ mice were sterile because of testicular atrophy starting at 5 wk of age, associated with degeneration of seminiferous tubules and the progressive loss of germ cells. Sustained WNT/CTNNB1 pathway activation was obtained in Ctnnb1 tm1Mmt/+;Amhr2 tm3(cre)Bhr/+ Sertoli cells. Sertoli cells often exhibited morphological characteristics suggestive of incomplete differentiation that appeared in a manner coincident with germ cell loss, accompanied by an increase in the expression of the immature Sertoli cell marker AMH. Microarray analyses performed on cultured Sertoli cells showed that CTNNB1 induces the expression of genes associated with the female sex determination pathway as well as cell-cycle associated genes . Together, these data suggest that the WNT/CTNNB1 pathway regulates Sertoli cell functions critical to their capacity to support spermatogenesis and to proliferate in the postnatal testis. Sertoli cells were obtained from 3wks-old Ctnnb1(tm1Mmt/tm1Mmt) mice. Cells were infected with adenoviruses to express eGFP or Cre in serum-free medium, and subsequently harvested for RNA extraction. Preliminary experiments demonstrated that an infection efficiency of nearly 100% could be obtained at an MOI of 50 (as determined by analysis of fluorescent signal in Ad-eGFP-infected cells) and that the Ad-Cre virus produced complete recombination of the floxed Ctnnb1 allele after 12 hours. Microaaray analyses were done using triplicate RNA samples from each adenoviral treatment using MouseRef-6 v.2.0 expression BeadChips technology (Illumina, San Diego, CA).

2011-04-05 | E-GEOD-28402 | biostudies-arrayexpress

Seminiferous tubule degeneration and infertility in mice with sustained activation of WNT/CTNNB1 signaling in sertoli cells

2011-04-05 | GSE28402 | GEO

Effect of WNT hyperactivation by CTNNB1 overexpression or APC knockdown on gene expression in HT29 cells

Project description:To investigate effect of WNT hyperactivation by CTNNB1 overexpression or APC knockdown on gene expression and probe possible mechanism of cell viability effect, we overexpressed GFP/CTNNB1, or induce knockdown of APC by shNT1 (non-targeting) and shAPC

2023-07-17 | GSE232944 | GEO

Changes in the transcriptome of primary mouse mammary gland organoids in response to hyperactivation of the WNT/CTNNB1 pathway

Project description:Purpose: WNT/CTNNB1 signaling promotes mammary tumor formation in mice, but the direct and immediate effects of elevated levels of WNT/CTNNB1 signaling on the mouse mammary epithelium remain unknown. Using primary mouse mammary epithelial organoid cultures grown in minimal media we have studied the response of the mouse mammary epithelium to elevated levels of WNT/CTNNB1 signaling.

2021-06-22 | GSE178321 | GEO

CTNNB1 mutations and overexpression of Wnt/beta-catenin target genes in WT1-mutant Wilms' tumors

Project description:Gain-of-function mutations in exon 3 of beta-catenin (CTNNB1) are specific for Wilms' tumors that have lost WT1, but 50% of WT1-mutant cases lack such "hot spot" mutations. To ask whether stabilization of beta-catenin might be essential after WT1 loss, and to identify downstream target genes, we compared expression profiles in WT1-mutant versus WT1 wild-type Wilms' tumors. Supervised and nonsupervised hierarchical clustering of the expression data separated these two classes of Wilms' tumor. The WT1-mutant tumors overexpressed genes encoding myogenic and other transcription factors (MOX2, LBX1, SIM2), signaling molecules (TGFB2, FST, BMP2A), extracellular Wnt inhibitors (WIF1, SFRP4), and known beta-catenin/TCF targets (FST, CSPG2, CMYC). Beta-Catenin/TCF target genes were overexpressed in the WT1-mutant tumors even in the absence of CTNNB1 exon 3 mutations, and complete sequencing revealed gain-of-function mutations elsewhere in the CTNNB1 gene in some of these tumors, increasing the overall mutation frequency to 75%. Lastly, we identified and validated a novel direct beta-catenin target gene, GAD1, among the WT1-mutant signature genes. These data highlight two molecular classes of Wilms' tumor, and indicate strong selection for stabilization of beta-catenin in the WT1-mutant class. Beta-Catenin stabilization can initiate tumorigenesis in other systems, and this mechanism is likely critical in tumor formation after loss of WT1. Keywords: single channel

2006-10-28 | GSE6120 | GEO

Transcriptomic analysis of gastric cancer cells in response to stable over-expression of circular RNA derived from CTNNB1 gene (circ-CTNNB1)

Project description:Circular RNAs (circRNAs), a subclass of noncoding RNAs characterized by covalently closed continuous loops, play emerging roles in tumorigenesis and aggressiveness. However, the functions and underlying mechanisms of circRNAs in regulating the Wnt/β-catenin signaling and cancer progression still remain elusive. We identify one intronic circRNA derived from CTNNB1 (circ-CTNNB1) as a novel driver of cancer progression. To investigate the mechanisms underlying the oncogenic functions of circ-CTNNB1, we employed the Illumina HiSeq X Ten as a discovery platform to analyze the transcriptome profiling changes of human gastric cancer AGS cells in response to stable over-expression of circ-CTNNB1. The results showed that stable over-expression of circ-CTNNB1 led to altered expression of 2230 human mRNAs, including 1244 up-regulated genes and 986 down-regulated genes. Furthermore, we validated the RNA-seq results by real-time RT-PCR with high identity. Overall, our results provided fundamental information about the transcriptomic changes in response to circ-CTNNB1 over-expression in human cancer cells, and these findings will help us understand the pathogenesis of cancer progression.

2019-09-30 | GSE120496 | GEO

Ctnnb1-targeted genes in mouse post-meiotic germ cells

Project description:To determine differential gene expression in Ctnnb1 CKO mice testis compared to CTRL mice testis. The Agilent Mouse Whole Genome 4x44K array (Samples are from pooled total testes RNA from 4 CTRL and 4 Ctnnb1 CKO mice; dye-swap was performed.)

2012-03-20 | E-GEOD-30773 | biostudies-arrayexpress

Combination CDC-like kinase inhibition (CLK) and taxane therapy in CTNNB1-mutated endometrial cancer

Project description:SM08502 is a novel pan CDC-like kinase (CLK) inhibitor that targets mRNA splicing and is optimized for Wnt pathway inhibition. Previous evaluation of single agent CLK inhibition (SM04690) demonstrated inhibition of tumor progression and b-catenin/TCF transcriptional activity in CTNNB1-mutant endometrial cancer (EC). In-vitro analysis of SM08502 similarly decreases Wnt transcriptional activity and cellular proliferation while increasing cellular apoptosis. Examining transcriptomic analysis, SM08502 increases pathways involved in RNA metabolism and spliceosome. Examining alternative splicing (AS) events, SM08502 increased differential splicing compared to treatment with paclitaxel. AS regulation is an important post-transcriptional mechanism associated with the oncogenic process in many cancers, including EC.

2023-08-07 | GSE215975 | GEO

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