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Beta-catenin target genes in colorectal carcinoma cell lines with deregulated Wnt/beta-catenin signaling

ABSTRACT: To validate the suitability of two commonly used colorectal cancer cell lines, DLD1 and SW480, as model systems to study colorectal carcinogenesis, we treated these cell lines with beta-catenin siRNA and identified beta-catenin target genes using DNA microarrays. The list of identified target genes was compared to previously published beta-catenin target genes found in the PubMed and the GEO databases. Based on the large number of beta-catenin target genes found to be similarly regulated in DLD1, SW480 and LS174T as well as the large overlap with confirmed β-catenin target genes, we conclude that DLD1 and SW480 colon carcinoma cell lines are suitable model systems to study beta-catenin regulated genes and signaling pathways 12 arrays (2 cell lines, 2 treatments, 3 biological replicates)

ORGANISM(S): Homo sapiens

SUBMITTER: Stefan Krebs

PROVIDER: E-GEOD-44097 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Comprehensive analysis of β-catenin target genes in colorectal carcinoma cell lines with deregulated Wnt/β-catenin signaling.

Herbst Andreas A Jurinovic Vindi V Krebs Stefan S Thieme Susanne E SE Blum Helmut H Göke Burkhard B Kolligs Frank T FT

BMC genomics 20140128

<h4>Background</h4>Deregulation of Wnt/β-catenin signaling is a hallmark of the majority of sporadic forms of colorectal cancer and results in increased stability of the protein β-catenin. β-catenin is then shuttled into the nucleus where it activates the transcription of its target genes, including the proto-oncogenes MYC and CCND1 as well as the genes encoding the basic helix-loop-helix (bHLH) proteins ASCL2 and ITF-2B. To identify genes commonly regulated by β-catenin in colorectal cancer cel ...[more]

PMID: 24467841

Similar Datasets

β-catenin target genes in colorectal carcinoma cell lines with deregulated Wnt/β-catenin signaling

Project description:To validate the suitability of two commonly used colorectal cancer cell lines, DLD1 and SW480, as model systems to study colorectal carcinogenesis, we treated these cell lines with β-catenin siRNA and identified β-catenin target genes using DNA microarrays. The list of identified target genes was compared to previously published β-catenin target genes found in the PubMed and the GEO databases. Based on the large number of β-catenin target genes found to be similarly regulated in DLD1, SW480 and LS174T as well as the large overlap with confirmed β-catenin target genes, we conclude that DLD1 and SW480 colon carcinoma cell lines are suitable model systems to study β-catenin regulated genes and signaling pathways

2013-12-31 | GSE44097 | GEO

FOXO3a and beta-catenin transcriptional profile in human colon cancer cell line DLD1

Project description:We established a model system in human DLD1 colon cancer cells to study the transcriptional crosstalk between FOXO3A and beta-Catenin. Thereby, translocation to the nucleus of a AKT-insensitive mutant (T32A, S253A, S315A) of human FOXO3A fused to the ligand binding domain of human estrogen receptor can be induced by exposure to 4-hydroxy-tamoxifen. Furthermore, expression of a stable mutant (S33Y) of human beta-catenin is doxycycline inducible. Addition of those drugs separately or in combination allows identification of common or excusive target gene sets.

2012-05-01 | E-MEXP-3262 | biostudies-arrayexpress

Mapping of the nuclear PI(3,4,5)P3 interactome in DLD1 and SW480 cells

Project description:Phosphatidylinositol (3,4,5)-trisphosphate (PI(3,4,5)P3) is a lipid second messenger produced by class I phosphoinositide 3-kinases (PI 3-kinases) phosphorylation of phosphatidylinositol (4,5)-bisphosphate (PI(4,5)P2). Although typically associated with the plasma membrane, it is now appreciated that PI(3,4,5)P3 generation also occurs in the nucleus to regulate a variety of biological functions. Using a PI(3,4,5)P3-specific GST-GRP1PH domain reporter and immunofluorescence microscopy, we have found that DLD1 and SW480 colorectal cancer (CRC) cells exhibit pronounced nuclear staining of PI(3,4,5)P3. To characterise the nuclear PI(3,4,5)P3 interactome in DLD1 and SW480 cells, we performed affinity pull-down experiments on nuclear extracts using a ω-amino analogue of phosphatidylinositol 3,4,5 -triphosphate (PI(3,4,5)P3 immobilised onto Affi-gel10 beads. Gel fractionation and LC/MS-MS analysis was performed to reduce sample complexity and increase resolution, with samples run on a LTQ Orbitrap Elite mass spectrometer. DLD1 and SW480 cells were both analysed in four independent biological replicates. A protein was considered a member of the nuclear PI(3,4,5)P3 interactome if it was identified in at least two experiments (with at least two peptides, FDR of 1%) in both cell lines, yielding a total of 1237 unique proteins (representing 1103 genes for DLD1 and 1001 genes for SW480 cells).

2023-05-10 | PXD021936 | Pride

Targeted disruption of the BCL9/beta-catenin complex in cancer

Project description:Stabilized Alpha-Helix peptides of BCL9 HD2 (SAH-BCL9) block BCL9 and B9L interactions with beta-catenin and specifically downregulate Wnt target gene expression. RNA from triplicate SAH-BCL9B- and vehicle-treated DLD1 samples (10 µM each for 12 hours) was hybridized to Affymetrix Human U133 Plus 2.0 arrays to asses global gene expression changes.

2012-08-23 | E-GEOD-33143 | biostudies-arrayexpress

Identification of beta-catenin binding regions in SW480 cells

Project description:Deregulation of canonical Wnt/beta-catenin pathway is one of the earliest events in the pathogenesis of colon cancer. Mutations in APC or CTNNB1 (beta-catenin gene) are highly frequent in colon cancer and cause aberrant stabilization of b-catenin, which activates the transcription of Wnt target genes by binding to chromatin via the TCF/LEF transcription factors. Here we report an integrative analysis of genome-wide chromatin occupancy of b-catenin by chromatin immunoprecipitation coupled with high-throughput sequencing (ChIP-seq) and gene expression profiling by microarray analysis upon RNAi-mediated knockdown of beta-catenin in colon cancer cells (GSE53656). Immunoprecipitated samples from human colon cancer SW480 cells with antibodies against beta-catenin and control IgG respectively were used for ChIP-seq experiments.

2014-03-12 | E-GEOD-53927 | biostudies-arrayexpress

Genome-scale CRISPR-Cas9 screen of Wnt/β-catenin signalling identifies therapeutic targets for Colorectal Cancer (ChIP-seq)

Project description:Using genome-scale CRISPR-Cas9 screening, our study revealed KMT2A as a critical regulator of β-catenin-driven CRC progression. To determine the role of KMT2A in β-catenin-mediated transcription, control and KMT2A-ablated DLD1 and SW480 colorectal cancer (CRC) cells were subjected to CHIP-seq analysis using anti-β-catenin and anti-H3K4me3 antibodies. Data obtained from the CHIP-seq experiments indicated a key role of KMT2A in β-catenin binding on active promoters.

2021-05-26 | GSE156081 | GEO

DLD1

Project description:DLD1 is an APC mut, KRAS mut, P53 mut CRC cell line. PROX1 transcription factor, target of Wnt pathway in CRC, is our protein of interest.DLD1 cells are PROX1 negative. We overexpressed through lentiviral expression PROX1 protein or the empty vector psd44, through selection of the cells in puromycin resistance. Afterwards we compared the transcriptional program of the DLD1-PROX1 and DLD1-Control cells growing in monolayer in vitro.

2014-09-18 | E-MTAB-2020 | biostudies-arrayexpress

Microarray analysis of beta-catenin regulated target genes in SW480 colon cancer cells

Project description:Deregulation of the canonical Wnt/beta-catenin pathway is one of the earliest events in the pathogenesis of colon cancer. Mutations in APC or CTNNB1 are frequent in colon cancer and cause aberrant stabilization of beta-catenin, which activates Wnt target genes by binding to chromatin via TCF/LEF transcription factors. In a comprehensive study, we conducted an integrative analysis of genome-wide chromatin occupancy of beta-catenin by chromatin immunoprecipitation coupled with high-throughput sequencing (ChIP-seq) along with gene expression profiling changes resulting from RNAi-mediated knockdown of beta-catenin in colon cancer cells. This experiment series represents the gene expression changes detected by microarray as a result of CTNNB1 perturbation. SW480 cells were transfected with control and beta-catenin siRNAs. Twenty-four hours after transfection, RNA was extracted from the cells using the RNeasy kit (Qiagen, Valencia, CA) and genome-wide cDNA microarray expression analysis was performed. The data reported here are the microarray data as processed by the standard Rosetta Resolver(R) ratio method for Agilent microarrays.

2013-12-27 | E-GEOD-53656 | biostudies-arrayexpress

Beta-catenin/LEF-1 induced epithelial-mesenchymal transition in DLD1 colon carcinoma cells

Project description:Our goal was to assess gene expression changes that occur when Lymphoid Enhancer Factor-1 (LEF-1) promotes epithelial-mesenchymal transition (EMT), the primary mechanism of tumor metastasis. To observe this phenomenon without interference from other signaling pathways, we selected DLD1 colon carcinoma cells (ATCC) which contain a mutation in APC. APC is a necessary component of a ubiquitin protein complex (including GSK-3beta, Axin, etc.) that is responsible for degrading cytoplasmic beta-catenin. Therefore, sufficient levels of LEF-1 can be easily activated by forming complexes with the abundant beta-catenin located in the cytoplasm of DLD1 cells. These complexes can then promote transcription of genes that stimulate EMT. We treated DLD1 cells with an adenoviral LEF-1 expression construct, which induced EMT within 48 hours. RNA was then extracted from these cells along with untreated DLD1 cells, then subjected to microarray analysis. From this analysis, we acquired several gene expression profiles by which epithelial colon carcinoma cells transform to an invasive, mesenchymal phenotype to initiate metastasis. Keywords: epithelial-mesenchymal transition, tumor metastasis, cancer progression, epithelial cell plasticity

2006-06-01 | GSE3229 | GEO

Transcription profiling of human DLD1 colon carcinoma cells treated with LEF-1 expression construct to examine Beta-catenin/LEF-1 induced epithelial-mesenchymal transition in DLD1 colon carcinoma cells

Project description:Our goal was to assess gene expression changes that occur when Lymphoid Enhancer Factor-1 (LEF-1) promotes epithelial-mesenchymal transition (EMT), the primary mechanism of tumor metastasis. To observe this phenomenon without interference from other signaling pathways, we selected DLD1 colon carcinoma cells (ATCC) which contain a mutation in APC. APC is a necessary component of a ubiquitin protein complex (including GSK-3beta, Axin, etc.) that is responsible for degrading cytoplasmic beta-catenin. Therefore, sufficient levels of LEF-1 can be easily activated by forming complexes with the abundant beta-catenin located in the cytoplasm of DLD1 cells. These complexes can then promote transcription of genes that stimulate EMT. We treated DLD1 cells with an adenoviral LEF-1 expression construct, which induced EMT within 48 hours. RNA was then extracted from these cells along with untreated DLD1 cells, then subjected to microarray analysis. From this analysis, we acquired several gene expression profiles by which epithelial colon carcinoma cells transform to an invasive, mesenchymal phenotype to initiate metastasis. Experiment Overall Design: DLD1 cells were treated with an adenoviral LEF-1 expression construct as described by Kim et al. (2002). Total RNA was extracted from both untreated and treated DLD1 cells using the RNeasy mini extraction kit (Qaigen). RNA amplification, biotin labeling, microarray hybridization, and fluidics were performed following the eukaryotic sample and array processing protocol (Affymetrix). Chips were scanned using an Affymetrix Gene Array Scanner (Hewlett-Packard). Raw data was compiled using Microarray Suite 5.0 software (Affymetrix).

2008-06-12 | E-GEOD-3229 | biostudies-arrayexpress

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