Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA767531 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13325908_1.fastq.gz | Fastqsanger.gz | |||
| SRR13325908_2.fastq.gz | Fastqsanger.gz | |||
| SRR13325911_1.fastq.gz | Fastqsanger.gz | |||
| SRR13325911_2.fastq.gz | Fastqsanger.gz | |||
| SRR13325914_1.fastq.gz | Fastqsanger.gz |
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Project description:Whole exome sequencing of colon tumors derived from Apc (Min716/+) transgenic mice under variant infection conditions
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Project description:Adenomatous polyposis coli (APC) is an important tumor suppressor and most directly related to the regulation of WNT/β-catenin signaling pathway. APC mutation has been identified as an early event in more than 80% of sporadic colorectal cancers (CRCs). However, obvious prognostic differences are observed in CRC patients with APC mutations. Although previous genomics has investigated the roles of concomitant gene mutations in determining the phenotypic heterogeneity of APC-mutant tumors, valuable prognostic determinants for APC-mutant CRC patients are still lacking. By using combined proteome and phosphoproteome, we classified the APC-mutant colon cancer patients and revealed the genomic, proteomic and phosphoproteomic heterogeneity in APC-mutant tumors. Of importance, we identified RAI14 as a key prognostic determinant for APC-mutant colon cancer patients, but not for APC-wildtype colon cancer patients. The heterogeneity and prognostic biomarkers in APC-mutant tumors were further confirmed in Clinical Proteomic Tumor Analysis Consortium (CPTAC) colon cancer cohort. In addition, we found that knockdown of RAI14 in cell lines led to reduced cell migration and changes in some epithelial-mesenchymal transition (EMT)-related markers. Mechanistically, knockdown of RAI14 was able to remodel the phosphoproteome associated with cell adhesion, which might promote F-action degradation and alter the expression of certain EMT markers. Collectively, this work describes the phenotypic heterogeneity of APC-mutant tumors and identifies the prognostic determinants for APC-mutant colon cancer patients. The prognostic utility of RAI14 in APC-mutant colon cancer will provide early warning and increase the chance of successful treatment.
2022-11-10 | PXD038081 |
Project description:Colon tumors in mice were generated by deleting one allele of the Apc gene, or both alleles of Tgif1 and Tgif2, together with a single Apc allele. Gene expression was compared by RNA-seq analysis of wild type colon, Apc mutant tumors or Apc mutant colon tumors with deletion of both Tgif1 and Tgif2. Comparison of Apc tumors to Apc;Tgif1;Tgif2 tumors was used to identify Tgif-dependent gene expression changes associated with intestinal tumorigenesis.
2019-04-10 | GSE116578 | GEO
Project description:Exome sequencing of iPSC-like cell lines derived from colon tumors in Apc min mouse model
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Project description:Mutated cells undergo changes in chromatin accessibility and gene expression, resulting in aberrant proliferation and differentiation, although how this occurs is unclear. HMGA1 chromatin regulators are abundant in stem cells and oncogenic in diverse tissues; however, their role in colon tumorigenesis is only beginning to emerge. Here, we uncover a previously unknown epigenetic program whereby HMGA1 amplifies Wnt signaling during colon tumorigenesis driven by inflammatory microbiota and/or Adenomatous polyposis coli (Apc) inactivation. Mechanistically, HMGA1 “opens” chromatin to up-regulate the stem cell regulator, Ascl2, and downstream Wnt effectors, promoting stem and Paneth-like cell states while depleting differentiated enterocytes. Loss of just one Hmga1 allele within colon epithelium restrains tumorigenesis and Wnt signaling driven by mutant Apc and inflammatory microbiota. However, HMGA1 deficiency has minimal effects in colon epithelium under homeostatic conditions. In human colon cancer cells, HMGA1 directly induces ASCL2 by recruiting activating histone marks. Silencing HMGA1 disrupts oncogenic properties, whereas re-expression of ASCL2 partially rescues these phenotypes. Further, HMGA1 and ASCL2 are co-expressed and up-regulated in human colorectal cancer. Together, our results establish HMGA1 as an epigenetic gatekeeper of Wnt signals and cell state under conditions of APC inactivation, illuminating HMGA1 as a potential therapeutic target in colon cancer.
2025-02-05 | GSE279070 | GEO
Project description:Mutated cells undergo changes in chromatin accessibility and gene expression, resulting in aberrant proliferation and differentiation, although how this occurs is unclear. HMGA1 chromatin regulators are abundant in stem cells and oncogenic in diverse tissues; however, their role in colon tumorigenesis is only beginning to emerge. Here, we uncover a previously unknown epigenetic program whereby HMGA1 amplifies Wnt signaling during colon tumorigenesis driven by inflammatory microbiota and/or Adenomatous polyposis coli (Apc) inactivation. Mechanistically, HMGA1 “opens” chromatin to up-regulate the stem cell regulator, Ascl2, and downstream Wnt effectors, promoting stem and Paneth-like cell states while depleting differentiated enterocytes. Loss of just one Hmga1 allele within colon epithelium restrains tumorigenesis and Wnt signaling driven by mutant Apc and inflammatory microbiota. However, HMGA1 deficiency has minimal effects in colon epithelium under homeostatic conditions. In human colon cancer cells, HMGA1 directly induces ASCL2 by recruiting activating histone marks. Silencing HMGA1 disrupts oncogenic properties, whereas re-expression of ASCL2 partially rescues these phenotypes. Further, HMGA1 and ASCL2 are co-expressed and up-regulated in human colorectal cancer. Together, our results establish HMGA1 as an epigenetic gatekeeper of Wnt signals and cell state under conditions of APC inactivation, illuminating HMGA1 as a potential therapeutic target in colon cancer.
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Project description:We thought the immediate effects of APC inactivation may represent unexplored therapeutic vulnerabilities in later stages of advanced colorectal adenocarcinoma. We performed transcriptome profiling of epithelial colon organoids immediately after APC inactivation and cross-referenced gene expression changes to the transcriptomes of several mouse models of colon cancer, including colon tumors in an inflammation-induced CRC model (AOM-DSS), a model of familial adenomatous polyposis (FAP, the Apcmin mouse), and an implantation-based model of metastatic adenocarcinoma using Apc/Trp53/KrasG12D/Smad4 quadruple-mutant tumor organoids15 (APKS tumoroids). Of the roughly 150 genes whose expression is acutely induced upon APC loss and remains elevated in these colon cancer models.
2022-12-31 | GSE198758 | GEO
Project description:This experiment was done to analyze the p53 status in gastrointestinal tumors in the colon and small intestine in APC mice carrying either a wild type p53 or a mutant p53 (R172H) allele and compare colon and small intestine tumors.
2020-02-25 | E-MTAB-8355 | biostudies-arrayexpress
Project description:Female MMTV/c-MYC transgenic mice expressed the c-MYC proto-oncogene or a more stable point mutation variant (T58A) of the gene under the control of the hormone-responsive MMTV long terminal repeat (LTR) in an FVB/NJ background (Jackson Laboratories, Bar Harbor, ME). The hormones released during pregnancy and lactation have been shown to enhance expression of the oncogene. Thus, the mice were maintained in a continuous breeding program. Mice were monitored twice weekly for tumor development by palpation and tumors were measured twice weekly. Once the tumors reached 3cm3 the animals were sacrificed and tissue was obtained to confirm the tumors by histological analysis. As a control, female mice of the same age and background strain were maintained in the same facility and under the same breeding conditions as their transgenic counterparts.
2011-03-01 | GSE27563 | GEO
Project description:Aberrant activation of the canonical Wnt pathway underlines the development and growth of intestinal tumors. The Apc-min (multiple intestinal neoplasia) mouse strain carries a single nucleotide mutation in one allele of the Apc tumor suppressor gene. Random deactivation of the second allele occurs during the life and results in the formation of multiple adenomas in the small intestine with occasional colonic occurence. The Defa6 promoter is active in adult small intestinal Paneth cells and its activation has been observed also in human colonic adenomas. To investigate the nature of Defa6+ colon adenoma cells, we used the Apc-min Rosa26-tdTomato Defa6-iCre mouse strain. In this strain, cells with an active Defa6 promoter are marked by expression of a red fluorescent protein (tdTomato). We performed gene expression profiling of Defa6-tdTomato+ cells isolated from mouse colon tumors.
2025-04-01 | E-MTAB-13752 | biostudies-arrayexpress