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.
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.
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.
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.
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.
Project description:In this study, we investigated the role of LIN28 in intestinal tumor initiation and invasive progression. We generated animal models with just intestinal LIN28B overexpression, or in combination with Apcmin/+ background. The animals develop intestinal and colorectal tumors with histology ranging from adenoma to adenocarcinoma. total RNA isolated from mouse small intestinal tumors with LIN28B overexpression, or duodenum and colon Apcmin tumors and LIN28B;Apcmin tumors
Project description:Background and aims: The transcription factor Stat3 has been considered to promote progression and metastasis of intestinal cancers. Methods: We investigated the role of Stat3 in intestinal tumors using mice with conditional ablation of Stat3 in intestinal epithelial cells (Stat3deltaIEC). Results: In the APCmin mouse model of intestinal cancer, genetic ablation of Stat3 reduced the multiplicity of early adenomas. However, loss of Stat3 promoted tumor progression at later stages leading to formation of invasive carcinomas which significantly shortened the lifespan of Stat3deltaIEC APCmin/+ mice. Interestingly, loss of Stat3 in tumors of APCmin/+ mice had no significant impact on cell survival and angiogenesis but promoted cell proliferation. A genome-wide expression analysis of Stat3-deficient tumors suggested that Stat3 negatively regulates intestinal cancer progression via the cell adhesion molecule Ceacam1. Conclusions: Our data suggest that Stat3 impairs progression of intestinal tumors. Therefore, detrimental effects on tumor progression have to be considered upon therapeutic targeting of the Stat3 signaling pathway in intestinal cancer.
Project description:APCmin/+ mice develop spontaneous gastrointestinal polyposis due to a dominantly inhereited germline loss-of-function mutation in the tumor suppressor adenomatous polyposis coli (APC). Changes in intestinal immune activity have been documented to occur prior to the development of fulminate polyposis. Such changes are thought to contribute to disease development. We used microarrays to describe the changing intestinal transcriptional landscape in APCmin/+ mice. Whole transcriptome profiling from polypotic and nonpolypotic intestinal sections of APC/min+ mice were examined in the early stages of disease, and compared to normal intestinal sections from littermate matched wildtype B6 mice. Nonpolypotic (wildtype and APCmin/+) and Polypotic (APCmin/+) sections of terminal ileum were identified by visual inspection, and subsequently selected for RNA isolation and hydridzation to Affymetrix Mouse Genome 430A 2.0 Arrays. Interference from bacterial RNA was selected against using a probeset enriched in oligos extending into 3’-poly-A tails.
