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Gene expression profiling of Trop2+ cells in mouse Apc-deficient small intestinal early adenomas

ABSTRACT: Gene expression profiling of Trop2+ cells in mouse Apc-deficient small intestinal early adenomas

PROVIDER: PRJEB50562 | ENA |

REPOSITORIES: ENA

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Gene expression profiling of Trop2+ cells in mouse Apc-deficient small intestinal early adenomas

Project description:Tumor Associated Calcium Signal Transducer 2 (TACSTD2) is one of the cancer-related genes whose overexpression correlates with tumor progression and invasiveness in human colorectal cancer. TACSTD2 gene encodes for a transmembrane glycoprotein TROP2, which is implicated in altered expression of epithelial-mesenchymal transition (EMT) markers and may play a role in metastasis formation. To determine how TROP2 affects aberrant tumor cell signaling, we isolated early adenoma cells from the mouse small intestine 6 weeks after disruption of the Adenomatous polyposis coli (Apc) gene, one of the first steps in the development of colorectal cancer in human. We performed expression profiling of Trop2+ and Trop2- tumor cells and, in addition, non-tumor cells of the intestinal epithelium, including predominantly differentiated cells.

2022-11-29 | E-MTAB-11382 | biostudies-arrayexpress

Gene expression profiling of Trop2+ cells in mouse Apc-deficient small intestinal hyperplastic epithelium

Project description:Tumor Associated Calcium Signal Transducer 2 (TACSTD2) is one of the cancer-related genes whose overexpression correlates with tumor progression and invasiveness in human colorectal cancer. TACSTD2 gene encodes for a transmembrane glycoprotein TROP2, which is implicated in altered expression of epithelial-mesenchymal transition (EMT) markers and may play a role in metastasis formation. To monitor the onset of TROP2 in hyperplastic cells and its effect on aberrant signaling potentially leading to tumor growth, we isolated epithelial cells from the mouse small intestine 7 days after disruption of the Adenomatous polyposis coli (Apc) gene. Loss of APC tumor suppressor function is the most common initial step in the development of colon cancer in humans. In the mice, the epithelial hyperproliferation occurs within a few days after Apc disruption, accompanied by the formation of ectopic crypts, followed by the formation of microadenomas over time. We performed expression profiling of Trop2+ and Trop2- hyperproliferating cells and, in addition, non-proliferating cells of the intestinal epithelium, including predominantly differentiated cells.

2022-11-29 | E-MTAB-11377 | biostudies-arrayexpress

Genome-wide mapping of Rad21 binding sites and gene expression profiling in wild type mouse small intestinal epithelial crypts and Apc Min adenomas

Project description:To investigate the role of RAD21 in the transcriptional regulation of global gene expression at early stage of colorectal cancer developments, we peformed the genome-wide analysis to map genomic regions bound by Rad21 in normal small testinal crypts and tumors (adenomas) harvested from Apc Min/+ mice using ChIP-seq. ChIP-seq naalysis identified high confidence RAD21 binding sites unique to normal crypts or adenomas, as well as those common to both tissues. We further performed RNA-seq to profile the changes in gene expression from normal WT crypts to adenomas at the very early stage of adenomagenesis in the context of Rad21 heterozygous loss. mRNA profiles of normal small intestinal crypts (WT) and adenomas from Apc Min/+ and Apc Min/+:Rad21+/- double mutant mouse; Mapping of Rad21 genomic binding sites in normal intestinal crypts (WT) and Apc Min/+ adenomas

2014-10-31 | E-GEOD-59283 | biostudies-arrayexpress

Gene expression profiling of Trop2+ cells in mouse Apc-deficient small intestinal hyperplastic epithelium

Project description:Gene expression profiling of Trop2+ cells in mouse Apc-deficient small intestinal hyperplastic epithelium

| PRJEB50466 | ENA

Transcriptional profiling of SI adenomas in Apc floxed mice

Project description:Small intestinal adenomas in mice with Apc deficiency following tamoxifen-induced genetic recombination.

2021-02-19 | GSE167008 | GEO

Genome-wide mapping of Rad21 binding sites and gene expression profiling in wild type mouse small intestinal epithelial crypts and Apc Min adenomas

2014-10-31 | GSE59283 | GEO

Intestinal IKKa is required for tumor initiation in APC mutant mice

Project description:We have generated a mouse model for tumor initiation carrying a mutation in APC and lacking IKKα in intestinal epithelial cells. IKKα-deficient intestinal cells primarily failed to generate adenomas, and the few adenomas arising in this background displayed a significant reduction in cell proliferation. Using an in vitro model for intestinal tumoroids (derived from adenoma initiating cells), we have performed RNA sequencing of wild type and IKKα-deficient intestinal tumoroids. This has demonstrated that epithelial IKKα controls transcription of stem cell-related genes and genes associated with proliferation and apoptosis.

2018-04-17 | GSE101415 | GEO

Transcriptional profiling of SI adenomas in Apc floxed mice

Project description:Transcriptional profiling of SI adenomas in Apc floxed mice

| PRJNA702654 | ENA

Transcription profiling by array of Apc-deficient mouse small intestinal epithelium upon Msx1 depletion.

Project description:The first step in the development of human colorectal cancer is the aberrant hyperactivation of the Wnt signaling pathway, predominantly caused by inactivating mutations in the adenomatous polyposis coli (Apc) gene encoding an essential tumor suppressor. The gene encoding transcriptional factor msh homeobox 1 (Msx1) displayed robust upregulation upon Apc inactivation in intestinal epithelium isolated in mice harboring the conditional allele of the Apc gene. To identify the gene signature in the small intestine upon Msx1 depletion, small intestinal epithelium from mice harboring conditional alleles of Apc and Msx1 was isolated and the gene expression profile was compared with control mice harboring the conditional allele of Apc only.

2019-11-01 | E-MTAB-6930 | biostudies-arrayexpress

Transcription profiling of transition from normal intestinal epithelia to adenomas and carcinomas in the APC(Min/+) mice to identify differentially expressed transcripts.

Project description:Transcriptional Profiling of the Transition from Normal Intestinal Epithelia to Adenomas and Carcinomas in the APC(Min/+) Mouse. Samples used in analysis:; * GSM6191-GSM6196 (WT): Ilea epithelial cells from C57/BL6 wild-type samples; * GSM6197-GSM6201 (Adenoma): Epithelial cells from crypts of adenomas of APC(Min/+) mice; * GSM6202-GSM6206 (Carcinoma): Epithelial cells from crypts of carcinomas of APC(Min/+) mice; Using a PixCell IIe instrument (Arcturus), ~30,000 laser firings per sample were used to collect cells of interest. RNA was extracted from captured cells by PicoPure (Arcturus) technique, followed by 2 rounds of RiboAmp amplification (Arcturus), with incorporation of biotinylated nucleotides (Enzo) in the IVT of round 2. All protocols were as per manufacturers instructions. 15ug of labeled cRNA from individual samples were hybridized to respective MG_U74Av2 chips (Affymetrix) and washed/stained using the standard EukGEWS2v4 protocol (Affymetrix). Chips were scanned and analyzed using MAS 5 (Affymetrix) and data scaled to TI=500. Pairwise comparisons using the Mann-Whitney test were performed in DMT 3 (Affymetrix), comparing WT vs Adenoma (n=6 x n=5; 83.3% concordance); WT vs Carcinoma (n=5 x n=5; 84% concordance); Adenoma vs Carcinoma (n=5 x n=5; 84% concordance). This resulted in the identification of differentially expressed transcripts. Fold changes were calculated from signal-log-ratios. Identified transcripts were clustered based on functional information which was publicly available at time of analysis, obtained through the NetAffx web portal (Affymetrix).

2007-11-06 | E-GEOD-422 | biostudies-arrayexpress

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