Browse
Submit Data
Databases
API
Help

Dataset Information

386 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Apc1638N+/- and p21-/- mouse models of colon cancer

ABSTRACT: DIGE results of mouse models of colon cancer. Tissue harvested from small intestines of Apc1638N+/- and p21-/- mice as per the method developed by Wieser et al. (1973). Spots identified as significant (alpha<0.05) in the comparison of mutant mouse crypts and villi to WT crypts and villi, respectively.

OTHER RELATED OMICS DATASETS IN: PRJNA121709

INSTRUMENT(S): LTQ Orbitrap, instrument model

ORGANISM(S): Mus Musculus (mouse)

SUBMITTER: Vishal Patel

PROVIDER: PRD000177 | Pride | 2012-05-02

REPOSITORIES: Pride

ACCESS DATA

Json Xml

Publications

Prediction and testing of biological networks underlying intestinal cancer.

Patel Vishal N VN Bebek Gurkan G Mariadason John M JM Wang Donghai D Augenlicht Leonard H LH Chance Mark R MR

PloS one 20100901 9

Colorectal cancer progresses through an accumulation of somatic mutations, some of which reside in so-called "driver" genes that provide a growth advantage to the tumor. To identify points of intersection between driver gene pathways, we implemented a network analysis framework using protein interactions to predict likely connections--both precedented and novel--between key driver genes in cancer. We applied the framework to find significant connections between two genes, Apc and Cdkn1a (p21), k ...[more]

PMID: 20824133

Similar Datasets

Expression data of small intestine crypts and villi from mice with nutritional and genetic risk factors for intestinal tumors

Project description:Nutritional and genetic risk factors for intestinal tumors are additive on mouse tumor phenotypes, demonstrating that diet and genetic factors impact risk by distinct combinatorial mechanisms. We analyzed expression profiles of small intestine crypts and villi from mice with nutritional and genetic risk factors. The results advanced our understanding of the mechanistic roles played by major risk factors in the pathogenesis of intestinal tumors. Small intestine crypts and villi from mice with nutritional (Ain76A, NWD1, and NWD2) and genetic risk factors (WT, Apc1638N/+ and p21-/-) were collected for RNA extraction and analysis using the Affymetrix 3' IVT expression microarray. Three or four replicates per tissue/risk factor.

2011-05-31 | E-GEOD-29538 | biostudies-arrayexpress

Spatial proteomics mouse intestine

Project description:Alcohol induced damages to teh crypts and villi of mouse small intestine revealed by laser capture microdissection (LCM)-based sample collection, DIA-based untargeted proteomics

2024-05-21 | PXD048687 | Pride

Transcription profiling of mouse small intestines

Project description:Rb and E2F are thought to play antagonistic roles in celll proliferation. However, this model is based mostly from in vitro cell culture systems. We used small intestines to test this model in vivo. We found that deletion of E2f1-3 in the small intestine of mice suppressed the ectopic expression of E2F targets and cell proliferation caused by Rb-deficiency. Surprisingly, E2f1-3 deletion failed to arrest the proliferation of intestinal cells containing an intact Rb gene, and instead led to E2F target derepression and apoptosis. Experiment Overall Design: Total RNA of crypts and villi from wild-type, Rb-/-, E2f1-/-, E2f2-/-, E2f3-/-, E2f1-/-, E2f2-/-, and E2f3-/- small intestines. Small intestines were harvested 7 days after mice were injected intraperitoneally with beta-napthoflavone.

2010-01-19 | E-GEOD-16454 | biostudies-arrayexpress

Gene expression profiles of irradiated WT and CREPT deleted intestinal epithelium

Project description:Intestinal stem cells (ISCs) residing in the crypts are critical for the continual self-renewal and rapid recovery of intestinal epithelium. The regulatory mechanism of ISCs is not fully understood. Here we report that CREPT, a recently identified tumor-promoting gene, is preferably expressed in the crypts, where the ISCs reside, but not in the villi. The Lgr5+ ISCs have much higher CREPT protein level than Lgr5- cells. To explore the function of CREPTduring regeneration, we isolated irradiated WT and CREPT deleted intestines (Vil-CREPTKO) to perform Next generation sequencing.

2020-11-08 | GSE143605 | GEO

Dynamic changes in chromatin states during specification and differentiation of adult intestinal stem cells [rnaseq]

Project description:To follow the changes in the transcriptional programs accompanying the specification, maintenance and differentiation of the adult ISCs we sequenced whole transcriptomes of embryonic intestinal epithelium progenitors (at E12.5 and E14.5), adult ISCs and their differentiated progenies, the majority of which are absorptive enterocytes. EpCAM positive embryonic gut epithelium was isolated from dissected small intestines using fluorescence activated cell sorting (FACS). Adult ISCs were purified on the basis of GFP fluorescence from crypts of Lgr5GFP-Cre-ERT mice (Barker et al. 2007), whereas enterocytes (EpCAM+ CD45- CD31-) were isolated from villi.

2017-03-29 | GSE89683 | GEO

Long-term in vitro expansion of epithelial organoids from human colon, adenoma, adenocarcinoma and Barrett's Esophagus

Project description:Background & Aims: We have recently established long-term culture conditions under which single crypts or stem cells derived from murine small intestine expand over long periods of time. Growing crypts undergo multiple crypt fission events, whilst simultaneously generating villus-like epithelial domains in which all differentiated cell types are present. We have now adapted the culture conditions to grow similar epithelial organoids from mouse colon and human small intestine and colon. Methods: Based on the murine small intestinal culture system, we optimized the murine and human colon culture system. Results: Addition of Wnt3A to the growth factor cocktail allowed mouse colon crypts to expand indefinitely. Further addition of nicotinamide, a small molecule Alk inhibitor and a p38 inhibitor was essential for long-term human small intestine and colon culture. The culture system also allowed growth of murine Apcmin adenomas, human colorectal cancer and human esophageal metaplastic Barrett’s epithelium. Conclusion: The culture technology should be widely applicable as a research tool for infectious, inflammatory and neoplastic pathologies of the human gastrointestinal tract. Moreover, regenerative applications may become feasible with ex vivo expanded intestinal epithelia. Human organoids were grown embedded in Matrigel in HISC (Human intestinal stem cell culture) medium. Additionally, human small intestinal crypts and villi were isolated independently from a freshly operated sample. RNA was isolated using the RNeasy Micro kit (Qiagen). Samples were labled according to Agilent guidelines with Cy3, whereas human reference RNA (Stratagene) was labeled in Cy5. Feature Extraction Software was used to extract and normalize data.

2011-12-07 | E-GEOD-28907 | biostudies-arrayexpress

Effect of CDK8/19 inhibitor Senexin A on p21-regulated gene expression in human HT1080 p21-9 cells with IPTG-inducible p21

Project description:p21 (CDKN1A) expression from an IPTG-inducible promoter in HT1080 p21-9 cells was previously shown to inhibit a set of genes, many of which are involved in cell cycle progression, and to upregulate another set of genes, some of which have been implicated in cancer and age-related diseases. We have now developed Senexin A, a small-molecule inhibitor of p21-induced transcription, which we found to be a selective inhibitor of CDK8 and CDK19. Here we tested the effect of Senexin A on the induction and inhibition of transcription by p21. In this dataset, we include microarray gene expression data from samples of HT1080 p21-9 cells that were either untreated, treated with p21-inducing IPTG alone, with Senexin A alone, or with IPTG and Senexin A. This experiment shows that Senexin A inhibits primarily the induction but not the inhibition of gene expression by p21. The data for each of the four samples were normalized to the sample from untreated cells, using GeneSpring GX. Fold changes in gene expression upon the addition of IPTG with or without Senexin A were compared using Microsft Excel. Changes in the expression of specific GO categories of genes were compared using GeneSpring.

2012-08-12 | E-GEOD-39464 | biostudies-arrayexpress

Effect of CDK8/19 inhibitor Senexin A on p21-regulated gene expression in human HT1080 p21-9 cells with IPTG-inducible p21

2012-08-13 | GSE39464 | GEO

The p53-regulated long noncoding RNA, lincRNA-p21 promotes the expression of Polycomb target genes and enforces the G1/S checkpoint by activating p21 in cis [ChIP-seq]

Project description:The p53-regulated long non-coding RNA, lincRNA-p21, has been proposed to promote apoptosis and to repress in trans the expression of genes in the p53 transcriptional network. Here, we report the generation of a conditional knockout mouse model developed to further examine lincRNA-p21 function. Using this genetic approach, we find that the primary function of lincRNA-p21 is to activate in cis the expression of its neighboring gene, the cyclin-dependent kinase inhibitor p21. Mechanistically, we show that lincRNA-p21 acts in concert with hnRNP-K as a co-activator for p53-dependent transcription of p21. Additional phenotypes of lincRNA-p21 deficiency, including deregulated expression and altered chromatin state of a set of Polycomb target genes, defective G1/S checkpoint, increased proliferation rates, and enhanced reprogramming efficiency could be attributed to diminished p21 levels. This study reveals a novel paradigm, whereby the long non-coding RNA lincRNA-p21 affects global gene expression and influences events in the p53 tumor suppressor pathway by acting in cis as a locus-restricted transcriptional co-activator for p53-mediated expression of p21. Examination of 2 different histone modifications (H3K4me3 and H3K27me3) in 2 cell types (WT and lincRNA-p21 KO) in the presence and absence of Doxorubicin.

2014-05-22 | E-GEOD-52956 | biostudies-arrayexpress

The p53-regulated long noncoding RNA, lincRNA-p21 promotes the expression of Polycomb target genes and enforces the G1/S checkpoint by activating p21 in cis [RNA-seq]

Project description:The p53-regulated long non-coding RNA, lincRNA-p21, has been proposed to promote apoptosis and to repress in trans the expression of genes in the p53 transcriptional network. Here, we report the generation of a conditional knockout mouse model developed to further examine lincRNA-p21 function. Using this genetic approach, we find that the primary function of lincRNA-p21 is to activate in cis the expression of its neighboring gene, the cyclin-dependent kinase inhibitor p21. Mechanistically, we show that lincRNA-p21 acts in concert with hnRNP-K as a co-activator for p53-dependent transcription of p21. Additional phenotypes of lincRNA-p21 deficiency, including deregulated expression and altered chromatin state of a set of Polycomb target genes, defective G1/S checkpoint, increased proliferation rates, and enhanced reprogramming efficiency could be attributed to diminished p21 levels. This study reveals a novel paradigm, whereby the long non-coding RNA lincRNA-p21 affects global gene expression and influences events in the p53 tumor suppressor pathway by acting in cis as a locus-restricted transcriptional co-activator for p53-mediated expression of p21. mRNAseq in 2 cell types (WT and lincRNA-p21 KO) in the presence and absence of Doxorubicin performed in biological triplicate.

2014-05-22 | E-GEOD-52957 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data