Project description:Intestinal crypts isolated from Apcflox/flox; villin-CreERT mice were treated with Tamoxifen to induce the deletion of Apc. Tamoxifen-treated organoids were selected in the absence of Wnt agonists and then treated with TGF-beta. Total RNA obtained from Tamoxifen-treated, Apc-deleted intestinal organoids in the absence or presence of 3 ng/ml TGF-beta (18h).
Project description:Gene expression changes in oncogenic Kras-containing, Apc-mutated mouse intestinal organoids in the presence or absence of TGF-beta
Project description:We isolated and selected intestinal adenoma organoids from Apc1638N/+ and Apc1638N/+; Kras mice. After the selection procedure, we maintained the cultures with or without TGF-beta for 18h. RNA was isolated to determine the effect of oncogenic Kras on the gene expression changes. Total RNA obtained from Apc1638N/+; Kras organoids were compared to Apc1638N/+ samples in the absence or presence of 3 ng/ml TGF-beta (18h).
Project description:Intestinal crypts isolated from Apcflox/flox; villin-CreERT mice were treated with Tamoxifen to induce the deletion of Apc. Tamoxifen-treated organoids were selected in the absence of Wnt agonists and then treated with TGF-beta.
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
Project description:We aimed to investigate gene expression changes in intestinal organoids from different mouse genotypes after treatment with TGF-beta. Wild-type, villinCreER;KrasG12D/+;Trp53fl/flRosa26N1icd/+ (KPN), and villinCreER;Apcfl/fl;KrasG12D/+;Trp53fl/flTgfbrIfl/fl (AKPT) intestinal organoids were plated, and the media was supplemented with 5ng/mL of recombinant mouse TGFß1 protein on Day 3. RNA was collected 24h later and processed for RNA sequencing.
Project description:We wanted to assess the role of Lef1 in ex vivo organoids using genetic mouse models of intestinal adenomas and scRNA-seq technology. Tumorigenesis was initiated by inducing Apc mutation in Lgr5+ stem cells. Intestinal cells of Lgr5-CreERT;Apc fl/fl (LApc) mouse and Lgr5-CreERT;Apc fl/fl; Lef1 fl/fl (LApcL) mouse were used to generate adenoma organoids. Organoids were cultured without growth factors for three passages and dissociated with Tryple express. We used WT mice as a control to distinguish adenoma cells. WT organoids were cultured with growth factors.
Project description:We isolated and selected intestinal adenoma organoids from Apc1638N/+ and Apc1638N/+; Kras mice. After the selection procedure, we maintained the cultures with or without TGF-beta for 18h. RNA was isolated to determine the effect of oncogenic Kras on the gene expression changes.
