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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE53656 | GEO | 2013/12/27

SECONDARY ACCESSION(S): PRJNA232592

REPOSITORIES: GEO

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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

Identification of beta-catenin binding regions in SW480 cells

2014-03-12 | GSE53927 | GEO

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

TCF/LEF dependent and independent regulation of Wnt/beta-catenin transcription

Project description:During canonical Wnt signalling the activity of nuclear beta-catenin is largely mediated by the TCF/LEF family of transcription factors. To challenge this view we used the CRISPR/Cas9 genome editing approach to generate HEK 293T cell clones simultaneously carrying loss-of-function alleles of all four TCF/LEF genes. Exploiting unbiased whole transcriptome sequencing studies, we found that a subset of beta-catenin transcriptional targets did not require TCF/LEF factors for their regulation. Consistent with this finding, we observed in a genome-wide analysis that beta-catenin occupied specific genomic regions in the absence of TCF/LEF. Finally, we revealed the existence of a transcriptional activity of beta-catenin that specifically appears when TCF/LEF factors are absent, and refer to this as beta-catenin-GHOST response. Collectively, this study uncovers a previously neglected modus operandi of beta-catenin that bypasses the TCF/LEF transcription factors.

2018-11-22 | E-MTAB-7028 | biostudies-arrayexpress

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BC ChIP-on-chip in SW480, array A

Project description:Dysregulation of Wnt signaling is involved in carcinogenesis, mainly through activation of beta-catenin/TCF target genes. Although aberrant activation of several Wnt target genes, including CCND1 and MYC, has been reported as promoting proliferation of cancer cells, it is hardly enough to understand malignant phenotypes of cancer cells with aberrant Wnt signaling. To elucidate the transcriptional regulation of beta-catenin/TCF target genes, we examined binding of beta-catenin (BC) to DNA by chromatin immunoprecipitation linked to genome tiling array (ChIP-on-chip).

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Non-coding RNAs Activated in Hepatoblastoma

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Expression data from human adrenocortical H295R cells expressing a doxycyclin-inducible shRNA targeting CTNNB1

Project description:We used the H295R cell line, human adrenocortical cells, harboring a heterozygous CTNNB1 (beta-catenin) gene mutation affecting the GSK3 beta-phosphorylation site (S45P) and leading to constitutive transcriptional activity of beta-catenin-LEF/TCF. Whole-transcript gene expression was analyzed in three stable clones of H295R cells expressing a doxycycline-inducible shRNA targeting CTNNB1 mRNA and in a control clone, without or with doxycycline for 5 days.

2015-08-03 | E-MTAB-3330 | biostudies-arrayexpress

Cell-line-specific gene expression changes following inactivation of the CTNNB1 gene in human colorectal cancer cell lines

Project description:Unrestrained transcriptional activity of β-CATENIN and its binding partner TCF7L2 frequently underlies colorectal tumor initiation and is considered an obligatory oncogenic driver throughout intestinal carcinogenesis. Yet, the TCF7L2 gene carries inactivating mutations in about 10 % of colorectal tumors and is non-essential in colorectal cancer (CRC) cell lines. To determine whether CRC cells acquire TCF7L2-independence through cancer-specific compensation by other T-cell factor (TCF)/lymphoid enhancer‑binding factor (LEF) family members, or rather lose addiction to β-CATENIN/TCF7L2-driven gene expression altogether, we generated multiple CRC cell lines entirely negative for TCF/LEF or β-CATENIN expression. Viability of these cells demonstrates complete β‑CATENIN- and TCF/LEF-independence, albeit one β-CATENIN-deficient cell line eventually became senescent. Absence of TCF/LEF proteins and β-CATENIN consistently impaired CRC cell proliferation, reminiscent of mitogenic effects of WNT/β-CATENIN signaling in the healthy intestine. Despite this common phenotype, β-CATENIN-deficient cells exhibited highly cell-line-specific gene expression changes with little overlap between β-CATENIN- and TCF7L2-dependent transcriptomes. Apparently, β‑CATENIN and TCF7L2 control sizeable fractions of their target genes independently from each other. The observed divergence of β-CATENIN and TCF7L2 transcriptional programs, and the finding that neither β-CATENIN nor TCF/LEF activity is strictly required for CRC cell survival has important implications when evaluating these factors as potential drug targets.

2022-12-13 | GSE199835 | GEO

The oncogene FOXQ1 is a selective activator of Wnt/β-catenin signalling

Project description:The forkhead box transcription factor FOXQ1 is aberrantly induced in various cancers, and contributes to tumour growth and metastasis. It has been suggested that the oncogenic potential of FOXQ1 may be explained by its activation of the Wnt/β-catenin signalling pathway.However, the mode of action of FOXQ1 in the Wnt pathway remains to be resolved. Here we report that FOXQ1 is bimodal transcriptional activator of Wnt target gene expression in normal and cancer cells. Using co-immunoprecipitation, proximity proteomics, and reporter assays, we show that FOXQ1 engages the Wnt transcriptional complex to promote gene expressionvia TCF/LEF transcription factors.

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