Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Atg7 deficiency induces a microbiome-influenced immune response and suppresses tumor growth to inhibit intestinal tumorigenesis

ABSTRACT: Here, we show that autophagy is activated in the intestinal epithelium in murine and human colorectal cancer and that the conditional inactivation of Atg7 in intestinal epithelial cells inhibits the formation of pre-cancerous lesions in Apc+/- mice by enhancing anti-tumor responses. The antibody-mediated depletion of CD8+ T cells showed that these cells are essential for the antitumoral responses mediated by the inhibition of autophagy. We show that Atg7 deficiency leads to intestinal dysbiosis and that the microbiota is required for anti-cancer responses. In addition, Atg7 deficiency resulted in a stress response accompanied by metabolic defects, AMPK activation and p53-mediated cell cycle arrest in tumor cells but not in normal tissue. This study reveals that the inhibition of autophagy within the epithelium may prevent the development and progression of colorectal cancer in genetically-predisposed patients.

ORGANISM(S): Mus musculus

PROVIDER: GSE56337 | GEO | 2015/05/26

SECONDARY ACCESSION(S): PRJNA242948

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Gene expression profiles in livers caused by Atg7 and/or Nrf2 deficiency

Project description:Autophagy deficiency caused by conditional knockout of Atg7 results in severe hepatitis accompanied by abundant accumulation of p62. p62 stablizes Nrf2 by disrupting the association between Keap1 and Nrf2. To understand the pathogenesis of hepatitis under the autophagy deficiency, we examined gene expression profiles of livers from Atg7-null, Nrf2-null and Atg7-Nrf2 double mutant mice. Eight week old Atg7F/F:Mx1-Cre mice and Atg7F/F:Mx1-Cre:Nrf2-/- together with control mice were injected with pIpC. At 4 weeks after pIpC injection, total RNAs were purified from each mouse liver.

2010-10-14 | E-GEOD-20415 | biostudies-arrayexpress

Gene expression profiles in livers caused by Atg7 and/or Nrf2 deficiency

2010-10-15 | GSE20415 | GEO

Microarray gene expression profiling from duodenum of Apc+/-Atg7-/- mice versus Apc+/- mice

Project description:we carried out microarray experiments to undestand how the inhibition of autophagy mediated by Atg7 deletion acts as tumor suppresion mechanism cDNA from duodenum of each genotype were prepared

2015-05-26 | E-GEOD-56337 | biostudies-arrayexpress

Expression data from NexCre:Atg7 conditional knockout mice brain

Project description:Transcriptome analysis of NesCre:Atg7 conditional knockout mice. Autophagy plays an important role in regulating protein metabolism and tissue homeostasis. Recent studies have reported that neural stem cell-specific Atg7 knockout mice (NesCre:Atg7f/f cKO mice) exhibit neonatal lethal due to severe neurodegeneration. However, the precise mechanisms of how neuronal fate is regulated by the autophagic pathway have not been elucidated. Here, we performed microarray experiments to analyze the changes in gene expression patterns in NesCre:Atg7 cKO mice. As a result, we could find a lot of candidate genes changed by Atg7 deficiency.

2022-10-07 | GSE214939 | GEO

ATG7(2) Interacts With Metabolic Proteins and Regulates Central Energy Metabolism

Project description:Macroautophagy/autophagy is a catabolic process that targets a wide variety of cellular components including proteins, lipids, damaged organelles, and pathogens. The autophagy protein ATG7 is involved in autophagy initiation by facilitating the lipidation of LC3/GABARAPs at the growing autophagosomal membrane. ATG7 is important for normal cellular homeostasis as well as diseased state such as tumor initiation and progression in various tumors. A short isoform of ATG7, termed ATG7(2) in contrast to the full-length ATG7(1), is unable to perform the characterized ATG7 mediated autophagy lipidation activity. In this study, we found that ATG7(1) and ATG7(2) are not correlated in expression in human tissues. They have different patterns of expression indicating that these isoforms are involved in diverse cellular mechanisms. To address the functional role of the short ATG7(2) isoform, we performed mass spectrometry analysis of the protein interactome of ATG7(1) and ATG7(2). This revealed that whereas ATG7(1) interacts with the autophagy machinery, ATG7(2) interacts with key glycolysis and mitochondrial membrane proteins. Functional experiments showed that ATG7(2) expression mediates a decrease in glycolytic activity, opposite to the effects mediated by ATG7(1) expression. These findings suggest a molecular switch between main catabolic processes through isoform dependent expression of a key autophagy gene.

2024-04-15 | PXD040548 | Pride

Bulk RNA-seq of primary visceral adipocytes isolated from wildtype mice or mice with adipocyte specific deletion of Atg7

Project description:Genes involved in the autophagic pathway are risk factors for the development of inflammatory bowel disease. In addition, patients with Crohn’s disease exhibit a profound expansion of mesenteric fat during the pathology. We investigated in our study the role of autophagy in mature adipocyte during intestinal inflammation. Mice bearing a tamoxifen-inducible deletion of Atg7 specifically in adipocytes showed signs of exacerbated intestinal inflammation in response to DSS-induced colitis. We therefore aimed to understand the possible underlying reasons for this change and performed a bulk RNA-seq approach using primary visceral adipocytes.

2023-01-14 | E-MTAB-12498 | biostudies-arrayexpress

Autophagy maintains intestinal stem cell integrity

Project description:The intestinal epithelium is continuously renewed by a pool of intestinal stem cells expressing Lgr5. We show that deletion of the key autophagy gene Atg7 affects the survival of Lgr5+ intestinal stem cells. Mechanistically, this involves defective DNA repair, oxidative stress, and altered interactions with the microbiota. This study highlights the importance of autophagy in maintaining the integrity of intestinal stem cells.

2020-05-28 | GSE136952 | GEO

Gene expression profiles in livers with conditional knock out of autophagy related protein 7 (Atg7)

Project description:Expression array analysis of mice livers with conditional deletion of autophagy related protein 7 (Atg7). Whole RNA from mice livers of 2 month old control (Atg7 FF), Olig1-CRE:Atg7 FF (conditional deletion in hepatocytes) and Alb-CRE:Atg7 FF (conditional deletion in hepatocytes/cholangiocytes) were analyzed. The results provide insight into the gene expression profile and role of autophagy in hepatocytes or hepatocytes/cholangiocytes in hepatic growth regulation and hepatocarcinogenesis.

2016-12-31 | GSE67676 | GEO

Expression data in antigen-specific CD8 T cells in the absence of ATG7

Project description:Autophagy genes play an important role in the T cell activation and proliferation. We examined the role of ATG7 during the process of CD8 T cell memory formation. In the absence of ATG7, antigen-specific CD8 T cells failed to survive past the contraction phase and failed to give rise to memory cells. We used microarrays to examine the global programme of gene expression underlying changes introduced in the absence of the ATG7 gene and identified distinct classes genes varied their expression during this time-point. Mouse LCMV-specific CD8 T cells were isolated at day 8 post LCMV infection for RNA extraction and hybridization on Affymetrix microarrays. We sought to compare the gene expression profiles in wild-type cells and cells lacking the ATG7 gene during the peak of their expansion.

2014-10-26 | E-GEOD-57047 | biostudies-arrayexpress

Comparison of expression data between control, Atg7, Bdh2, Atg7 and Bdh2 dual morphant zebrafish embryos

Project description:Bdh2 morphants displayed mitochondrial dysfunction and degradation by autophagy, as well as hypohemoglobinization. Suppression of Atg7 expression in Bdh2 morphants diminished mitochondrial clearance and partly corrected their hemoglobinization defect.

2016-01-21 | GSE76508 | GEO

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