Ontology highlight
ABSTRACT:
PROVIDER: PRJNA132419 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:This SuperSeries is composed of the following subset Series: GSE24575: Beta-arrestin-2 deficiency effect on intestinal tumorigenesis in Apc-mutated mice GSE24576: Gene expression analysis of tumors from ApcD14/+ mice Refer to individual Series
2012-01-20 | E-GEOD-24577 | biostudies-arrayexpress
Project description:beta-arrestin-2 deficiency effect on intestinal tumorigenesis in Apc-mutated mice
| PRJNA133595 | ENA
Project description:Amoung their pleiotropic functions, a role was recently assigned for b-arrestin scaffold proteins in tumor growth, angiogenesis and invasion. In order to elucidate the roles of b-arrestins in tumour developement in intestinal epithelium initiated by Apc mutation, we determined the effects of b-arrestin gene deletion on intestinal polypolis using ApcD14/+ mice, a relevant mouse model of human intestinal tumorigenesis.Here we show that unlike b-arrestin1, absence of b-arrestin2 dramatically decreased the number of spontaneously developping intestinal tumors in ApcD14/+ mice.The size of residual tumors was similarto that of controls, suggesting that their growth is b-arrestin2-independent. This result demonstrated a role for b-arrestin2 in the early development of a tumor subset. Gene expression profils analysis of ApcD14/+:Arrb2+/+ and ApcD14/+:Arrb2-/- tumors showed two distinct clusters among ApcD14/+:Arrb2+/+ tumors and one of them was statistically more correlated to ApcD14/+:Arrb2-/- tumors than to the other ApcD14/+:Arrb2+/+ cluster, eventhough a number of genes saw their expression affected in ApcD14/+:Arrb2-/- tumors only. Altogether, our data unravel an unexpected early diversity among intestinal tumors and a crucial role for b-arrestin2 in early tumor development in Apc-mutated mice. 16 tumors from ApcD14/+:Arrb2+/+ mice and 13 tumors from ApcD14/+:Arrb2-/- mice
2012-01-20 | E-GEOD-24575 | biostudies-arrayexpress
Project description:Amoung their pleiotropic functions, a role was recently assigned for b-arrestin scaffold proteins in tumor growth, angiogenesis and invasion. In order to elucidate the roles of b-arrestins in tumour developement in intestinal epithelium initiated by Apc mutation, we determined the effects of b-arrestin gene deletion on intestinal polypolis using ApcD14/+ mice, a relevant mouse model of human intestinal tumorigenesis.Here we show that unlike b-arrestin1, absence of b-arrestin2 dramatically decreased the number of spontaneously developping intestinal tumors in ApcD14/+ mice.The size of residual tumors was similarto that of controls, suggesting that their growth is b-arrestin2-independent. This result demonstrated a role for b-arrestin2 in the early development of a tumor subset. Gene expression profils analysis of ApcD14/+:Arrb2+/+ and ApcD14/+:Arrb2-/- tumors showed two distinct clusters among ApcD14/+:Arrb2+/+ tumors and one of them was statistically more correlated to ApcD14/+:Arrb2-/- tumors than to the other ApcD14/+:Arrb2+/+ cluster, eventhough a number of genes saw their expression affected in ApcD14/+:Arrb2-/- tumors only. Altogether, our data unravel an unexpected early diversity among intestinal tumors and a crucial role for b-arrestin2 in early tumor development in Apc-mutated mice. 10 tumors from 2 different ApcD14 mice
2012-01-20 | E-GEOD-24576 | biostudies-arrayexpress
Project description:APC is mutated in the majority of colorectal cancers. Inducible deletion of Apc in intestinal epithelial cells in Apcfl//fl; Villin-CreERT2 mice recapitulates this tumor-initiating mutation resulting in expanded intestinal crypts, including stem cells. We used microarrays to analyze BEC gene expression changes during the early stages of intestinal tumorigenesis.
2022-03-29 | GSE111783 | GEO
Project description:Transcription profiling of colonic mucosa of Apc Min/+ mice fed with maslinic acid (MA) to study the underlying mechanisms by which MA inhibits intestinal tumorigenesis
2015-11-02 | E-MTAB-4007 | ExpressionAtlas
Project description:Cited-1 deficiency suppresses intestinal tumorigenesis through the repression of the Wnt pathway- evidence for the just right model of Wnt mediated tumorigenesis
2015-10-22 | E-MEXP-3202 | ExpressionAtlas
Project description:Amoung their pleiotropic functions, a role was recently assigned for b-arrestin scaffold proteins in tumor growth, angiogenesis and invasion. In order to elucidate the roles of b-arrestins in tumour developement in intestinal epithelium initiated by Apc mutation, we determined the effects of b-arrestin gene deletion on intestinal polypolis using ApcD14/+ mice, a relevant mouse model of human intestinal tumorigenesis.Here we show that unlike b-arrestin1, absence of b-arrestin2 dramatically decreased the number of spontaneously developping intestinal tumors in ApcD14/+ mice.The size of residual tumors was similarto that of controls, suggesting that their growth is b-arrestin2-independent. This result demonstrated a role for b-arrestin2 in the early development of a tumor subset. Gene expression profils analysis of ApcD14/+:Arrb2+/+ and ApcD14/+:Arrb2-/- tumors showed two distinct clusters among ApcD14/+:Arrb2+/+ tumors and one of them was statistically more correlated to ApcD14/+:Arrb2-/- tumors than to the other ApcD14/+:Arrb2+/+ cluster, eventhough a number of genes saw their expression affected in ApcD14/+:Arrb2-/- tumors only. Altogether, our data unravel an unexpected early diversity among intestinal tumors and a crucial role for b-arrestin2 in early tumor development in Apc-mutated mice.
2012-01-20 | GSE24576 | GEO
Project description:Amoung their pleiotropic functions, a role was recently assigned for b-arrestin scaffold proteins in tumor growth, angiogenesis and invasion. In order to elucidate the roles of b-arrestins in tumour developement in intestinal epithelium initiated by Apc mutation, we determined the effects of b-arrestin gene deletion on intestinal polypolis using ApcD14/+ mice, a relevant mouse model of human intestinal tumorigenesis.Here we show that unlike b-arrestin1, absence of b-arrestin2 dramatically decreased the number of spontaneously developping intestinal tumors in ApcD14/+ mice.The size of residual tumors was similarto that of controls, suggesting that their growth is b-arrestin2-independent. This result demonstrated a role for b-arrestin2 in the early development of a tumor subset. Gene expression profils analysis of ApcD14/+:Arrb2+/+ and ApcD14/+:Arrb2-/- tumors showed two distinct clusters among ApcD14/+:Arrb2+/+ tumors and one of them was statistically more correlated to ApcD14/+:Arrb2-/- tumors than to the other ApcD14/+:Arrb2+/+ cluster, eventhough a number of genes saw their expression affected in ApcD14/+:Arrb2-/- tumors only. Altogether, our data unravel an unexpected early diversity among intestinal tumors and a crucial role for b-arrestin2 in early tumor development in Apc-mutated mice.
2012-01-20 | GSE24575 | GEO
Project description:Chemoprevention is a pragmatic approach to reduce the risk of colorectal cancer, one of the leading causes of cancer-related death in western countries. In this regard, maslinic acid (MA), a pentacyclic triterpene extracted from wax-like coatings of olives, is known to inhibit proliferation and induce apoptosis in colon cancer cell lines without affecting normal intestinal cells. The present study evaluated the chemopreventive efficacy and associated mechanisms of maslinic acid treatment on spontaneous intestinal tumorigenesis in Apc(Min/+) mice. Twenty-two mice were randomized into 2 groups: control group and MA group, fed with a maslinic acid-supplemented diet for six weeks. MA treatment reduced total intestinal polyp formation by 45% (P<0.01). Putative molecular mechanisms associated with suppressing intestinal polyposis in Apc(Min/+) mice were investigated by comparing microarray expression profiles of MA-treated and control mice and by analyzing the serum metabolic profile using NMR techniques. The different expression phenotype induced by MA suggested that it exerts its chemopreventive action mainly by inhibiting cell-survival signaling and inflammation. These changes eventually induce G1-phase cell cycle arrest and apoptosis. Moreover, the metabolic changes induced by MA treatment were associated with a protective profile against intestinal tumorigenesis. These results show the efficacy and underlying mechanisms of MA against intestinal tumor development in the Apc(Min/+) mice model, suggesting its chemopreventive potential against colorectal cancer.
2017-02-09 | MTBLS240 | MetaboLights