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Gene expression profiles of DLD1 cells in which GATA6 or LGR5 expression was suppressed.

ABSTRACT: Mutations in APC or β-catenin that cause aberrant activation of Wnt signaling are responsible for the initiation of colorectal tumor development. LGR5 is specifically expressed in stem cells of the intestine, stomach and hair follicle, and plays essential roles in maintaining tissue homeostasis. LGR5-positive stem cells have been shown to be responsible for the intestinal adenoma initiated by some mutations in APC . Furthermore, it has recently been reported that Lgr5, which is associated with the Frizzled/Lrp Wnt receptor complex, interacts with R-spondins and thereby activates Wnt signaling. However, the function of LGR5 in colorectal tumorigenesis has been unclear. Here we show that LGR5 is required for the tumorigenicity of colorectal cancer cells. We also show that the transcription factor GATA6 directly enhances the expression of LGR5. DLD1 cells were infected with a lentivirus expressing an shRNA targeting GATA6 or LGR5.

ORGANISM(S): Homo sapiens

SUBMITTER: Tetsu Akiyama

PROVIDER: E-GEOD-32987 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Gene expression profiles of DLD1 cells in which GATA6 or LGR5 expression was suppressed.

Project description:Mutations in APC or β-catenin that cause aberrant activation of Wnt signaling are responsible for the initiation of colorectal tumor development. LGR5 is specifically expressed in stem cells of the intestine, stomach and hair follicle, and plays essential roles in maintaining tissue homeostasis. LGR5-positive stem cells have been shown to be responsible for the intestinal adenoma initiated by some mutations in APC . Furthermore, it has recently been reported that Lgr5, which is associated with the Frizzled/Lrp Wnt receptor complex, interacts with R-spondins and thereby activates Wnt signaling. However, the function of LGR5 in colorectal tumorigenesis has been unclear. Here we show that LGR5 is required for the tumorigenicity of colorectal cancer cells. We also show that the transcription factor GATA6 directly enhances the expression of LGR5.

2011-10-18 | GSE32987 | 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

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

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

Apc-mutants act as supercompetitors in intestinal tumour initiation

Project description:Almost all colorectal cancers (CRC) present with mutations in the Apc gene, leading to unrestrained Wnt activation and the initiation of tumour development. We previously reported the competitive benefit of Apc-mutant intestinal stem cells (ISCs) within the crypt, however, the mechanism by which they outcompete their wild type (WT) neighbours remained elusive. Here, we studied the effect of Apc-mutants using an in vitro culture system of WT (Lgr5-CreErt2) and Apc-/- (Lgr5-CreErt2;Apcfl/fl) organoids . The expression patterns of WT and Apc-/- organoids revealed significant upregulation in specific secreted Wnt antagonists Notum, Wif1 and Dkk2. Furthermore, we studied the effect of the secreted antagonist by treating WT organoids with either WT or Apc-/- conditioned medium (CM) for 48 hours and observed a significant decrease in stem cell markers and an increase in goblet cell markers. We report that Apc-mutants act as bona fide supercompetitors by secreting Wnt antagonists that result in active differentiation of WT ISCs.

2021-03-25 | GSE144325 | GEO

Analyzing the effect of Lef1 deletion in mouse intestinal adenoma cells with single-cell RNA sequencing

Project description:Somatic mutations in APC or CTNNB1 genes lead to aberrant Wnt signaling and colorectal cancer (CRC) initiation and progression. Activation of Wnt pathway leads to the formation of beta-catenin-T-cell factor/Lymphoid enhancer binding factor 1 (Tcf/Lef1) complexes that activate transcription of oncogenic target genes. Lef1 is the only member of the Tcf gene family that is not expressed in the normal intestine, but is induced during intestinal tumorigenesis. Thus, we wanted to assess the role of Lef1 using genetic mouse models of intestinal adenomas and scRNA-seq technology. Tumorigenesis was initiated by inducing Apc mutation in Lgr5+ stem cells. Intestinal EpCAM+ epithelial cells of Lgr5-CreERT;Apc fl/fl (LApc) mouse and Lgr5-CreERT;Apc fl/fl; Lef1 fl/fl (LApcL) mouse were used to analyze the effects of Lef1 deletion in intestinal adenoma cells. We used WT mice as a control to distinguish adenoma cells.

2021-12-10 | GSE179483 | GEO

Human DLD1 Cells: shRNA_Control vs. shRNA_FOXQ1

Project description:Transcriptional profiling of human colorectal cell DLD1 transfected by shRNA_Control or shRNA_FOXQ1 respectively.

2015-10-22 | GSE74223 | GEO

Expression data from YAP-S127D DLD1 Xenografts

Project description:We overexpressed YAP-S127D in DLD1 colorectal cancer cells for 21 days after sub-cutaneous (SubQ) injection into the flanks of nude mice.

2012-11-29 | GSE41508 | GEO

Differential Gene expression of furin knockout (KO) DLD1, HCA7 and HT29 colorectal cancer cells

Project description:We created furin KO cells in three colorectal cancer cell lines (DLD1, HCA7 and HT29) using CRISPR-Cas9 genome editing. And then we performed RNA-Seq analysis in furin KO colorectal cancer cells to identify potential effect of furin on gene expression patterns in DLD1, HCA7 and HT29 cells.

2020-03-15 | GSE130969 | GEO

Gene expression profiles of HT29 cells in which LGR5 expression was suppressed.

Project description:GATA6 is a zinc finger transcription factor that is required for the proliferation, development and specific gene regulation in the gastrointestinal tract. We have recently reported that GATA6-mediated induction of the intestinal stem cell marker LGR5 is required for the tumorigenicity of colon cancer cells. However, knockdown of LGR5, unlike GATA6, does not affect the proliferation of these cells under adherent conditions. Here we show that REG4, a member of the regenerating islet-derived (REG) family, is a target of GATA6. We further demonstrate that REG4 is downregulated by overexpression of miR-363, which suppresses GATA6 expression. Moreover, we show that GATA6-mediated activation of REG4 causes an acceleration of the growth of colon cancer cells under adherent conditions. These results suggest that GATA6 simultaneously activates the transcription of genes required for growth (REG4) and clonogenicity (LGR5), and the miR-363-GATA6-REG4/LGR5 pathway is critical for colorectal tumorigenesis. HT29 cells were transfected with a siRNA targeting LGR5.

2016-06-15 | E-GEOD-62317 | biostudies-arrayexpress

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