Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA232592 | ENA |
REPOSITORIES: ENA
Similar Datasets
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
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 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)
2013-12-31 | E-GEOD-44097 | biostudies-arrayexpress
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
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
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).
2014-03-12 | GSE53927 | GEO
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.
2013-12-27 | GSE53656 | GEO
Project description:MiR-10a inhibits colon cancer invasion and metastasis. To search the candidate target genes of miR-10a, SW480 cells were transfected with miR-10a blockage to suppress miR-10a activity and the differentially expressed genes were detected by cDNA microarray analysis. Some of the up-regulated genes may be candidate target genes of miR-10a.
2009-02-20 | E-MEXP-2061 | biostudies-arrayexpress
Project description:To determine the critical mediator of TRIB3-enhanced Wnt/beta-catenin signaling, we examined the expression profile of genes that might regulate Wnt/beta-catenin by using mRNA microarrays. Aberrant activation of Wnt/beta-catenin signaling pathway is a major reason for the tumorigenesis of Colon cancer. However, no specific drug targeting this pathway has been in the market. Surgery combined with cytotoxic drugs are still the major therapy methods toward colon cancer. These highlighted the need for therapeutics with alternative mechanisms of action. Here we report that the elevated TRIB3 expression associates positively with Wnt/beta-catenin signaling pathway. TRIB3 interacts with beta-catenin and TCF4 to enhance the associations between TCF4/beta-catenin target genes’ promoters, which upregulates the transcriptional activity of beta-catenin, thus to promote the CSC stemness and colon cancer tumorigenesis.
2020-11-17 | GSE107094 | GEO
Project description:Beta-catenin-regulated genes in pancreatic cancer cells
| PRJNA325277 | ENA
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