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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Identification of beta-catenin binding regions in SW480 cells

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

SUBMITTER: Kazuhide Watanabe

PROVIDER: E-GEOD-53927 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Characterisation of the Beta-Catenin cytoplasmic/nuclear interactome in leukaemia cells

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Identification of beta-catenin binding regions in SW480 cells

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2014-03-12 | GSE53927 | GEO

CUT&RUN experiment at four time points in HEK293T and hESC cells, assessing the time-resolved response of β-catenin genomic occupancy upon Wnt signaling activation

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2022-09-30 | E-MTAB-12077 | 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

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