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PWD/Ph-encoded genetic variants suppress ApcMin-triggered intestinal tumor formation by modulating the cellular Wnt/beta-Catenin response

ABSTRACT: PWD/Ph-encoded genetic variants suppress ApcMin-triggered intestinal tumor formation by modulating the cellular Wnt/beta-Catenin response

PROVIDER: PRJNA624087 | ENA |

REPOSITORIES: ENA

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PWD/Ph-encoded genetic variants suppress ApcMin-triggered intestinal tumor formation by modulating the cellular Wnt/beta-Catenin response

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-03-20 | GSE148370 | GEO

Microarray analysis of ApcMin/+ and D6(ACKR2)-/-ApcMin/+ tumors

Project description:Mast cells have been suggested to either promote or suppress tumor progression but the mechanisms underlying these outcomes are unclear. Here, we show that mice with a heterozygous mutation in the adenomatous polyposis coli gene (ApcMin/+) displayed reduced intestinal tumor burden and increased survival in the background of the chemokine decoy receptor ACKR2 deficiency (ACKR2-/-). The ACKR2-/-ApcMin/+ tumors showed increased infiltration of mast cells. In mast cell-deficient Sash (c-kitW-sh/W-sh) ACKR2-/-ApcMin/+ mice the survival advantage was lost as the tumors grew rapidly and adoptive transfer of mast cells reduced the tumor burden in these mice. The tumor burden is also increased in Rag2-/-ACKR2-/-ApcMin/+ mice and the protection is reconstituted by adoptively transferred CD8+ T-lymphocytes. Mast cells from ACKR2-/- mice expressed elevated levels of chemokine receptors CCR2 and CCR5 and are also efficient in antigen presentation and activation of CD8+ T-cells. Mast cell-derived leukotriene B4 is a critical mediator of CD8+ T-lymphocyte recruitment as the BLT1-/-ACKR2-/-ApcMin/+ mice are highly susceptible to intestinal tumor induced mortality. Taken together, these data demonstrate that chemokine mediated mast cell recruitment is essential for initiating LTB4/BLT1 regulated CD8+ T-cell homing and generation of effective anti-tumor immunity against intestinal tumor development.

2017-12-31 | GSE104829 | GEO

Microarray analysis of ApcMin/+ and D6(ACKR2)-/-ApcMin/+ tumors

Project description:Microarray analysis of ApcMin/+ and D6(ACKR2)-/-ApcMin/+ tumors

| PRJNA413950 | ENA

Genome-wide analysis expression of ileum tumor samples from FVBN/APCmin and iPGC-1β/APCmin

Project description:Analysis of metabolic pathway gene expression. The hypothesis tested in the present study is to assess mRNA level changes in metabolic genes in intestinal tumors from APCmin mice overexpressing PGC-1β specifically in the intestine. Total RNA obtained from ileum tumor samples from iPGC-1β/APCmin mice was compared to the total RNA extracted from FVBN/APCmin mice.

2015-03-01 | E-GEOD-61642 | biostudies-arrayexpress

Genome-wide analysis of gene expression profile of Intestinal (ILEUM) Tumors from APCmin/+/VP16LXRa vs APCmin/+/VP16

Project description:Changes in gene expression profile of intestinal (ILEUM) Tumors from APCmin/+/VP16LXRa vs APCmin/+/VP16. The hypothesis tested in the present study was that LXRa overexpression influence cancer growth modulating lipid metabolism in cancer cells. Results provide the information that LXRa induces genes encoding proteins able to regulate cholesterol efflux. Total RNA obtained from Ileum tumors from APCmin/+/VP16LXRa mice was compared to total RNA extracted from APCmin/+/VP16 mice.

2013-02-05 | E-GEOD-44071 | biostudies-arrayexpress

Genome-wide analysis of gene expression profile of Intestinal (COLON) Tumors from APCmin/+/VP16LXRa vs APCmin/+/VP16

Project description:Changes in gene expression profile of intestinal (COLON) Tumors from APCmin/+/VP16LXRa vs APCmin/+/VP16. The hypothesis tested in the present study was that LXRa overexpression influence cancer growth modulating lipid metabolism in cancer cells. Results provide the information that LXRa induces expression of genes encoding proteins able to regulate cholesterol efflux. Total RNA obtained from colonic tumors from APCmin/+/VP16LXRa mice was compared to total RNA extracted from APCmin/+/VP16 mice.

2013-02-05 | E-GEOD-44070 | biostudies-arrayexpress

Intestinal cancer modifier MeDIP-Seq

Project description:Cancers predominantly arise from adult stem cells accumulating somatic driver mutations, but how genetic predisposition affects the penetrance of mutations in tumor initiation is not well understood. Here, we have analyzed gene expression in tumor-prone ApcMin/+ mice on highly variant C57BL/6J and PWD/Ph genetic backgrounds. We show that activation of beta-Catenin-driven and stem cell-specific gene expression in the presence of ApcMin or following APC loss is high in B6 mouse intestines, but remains moderate in intestines carrying PWD/Ph chromosome 5, suggesting that PWD/Ph variants restrict adenoma initiation by controlling stem cell homeostasis. Gene expression of modifier candidates and DNA methylation on chromosome 5 are predominantly cis-controlled and largely reflect the parental patterns, providing a genetic basis for inheritance of tumor susceptibility.

2023-03-20 | GSE148369 | GEO

Intestinal cancer modifier RNA-Seq

2023-03-20 | GSE148365 | GEO

miR-34a and miR-34b/c suppress intestinal tumorigenesis in ApcMin/+ Mice

Project description:miR-34a and miR-34b/c genes are frequently epigenetically silenced in primary CRCs. However, the in vivo relevance of miR-34a/b/c for suppression of intestinal tumor formation has not been analyzed by genetic approaches. ApcMin/+ mice with deletion of the miR-34a and miR-34b/c genes were generated and analyzed. The mRNA expression profiles of intestinal adenomas with and without functional miR-34a/b/c genes were compared.

2017-05-28 | GSE84138 | GEO

Expression data from small intestine crypts of Zfp148gt/+APCMin/+ and Zfp148+/+APCMin/+ mice

Project description:The transcription factor Zinc finger protein 148 (Zfp148) interacts physically with the tumor suppressor p53, but the siginficance of this interaction is not known. We recently showed that knockout of Zfp148 in mice leads to ectopic activation of p53 in tissues and cultured fibroblasts, suggesting that Zfp148 represses p53 activity. Here we hypothesized that targeting Zfp148 would unleash p53 activity and protect against cancer development, and test this idea in the APCMin/+ mouse model of intestinal adenomas. Crypt-enriched tissues were isolated by laser microdissection (PALM) from the small intestines (proximal) of Zfp148gt/+APCMin/+ and Zfp148+/+APCMin/+ mice for RNA extraction and hybridization to Affymetrix microarrays.

2016-02-10 | E-GEOD-77773 | biostudies-arrayexpress

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