Expression data from 6-month Helicobacter felis-infected WT and Gli1-/- mouse stomachs
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
SUBMITTER: Mohamad El-Zaatari
PROVIDER: E-GEOD-43693 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:Gli1 is necessary for the progression from chronic gastric inflammation to metaplasia in the stomach. We therefore compared the expression patterns between 6-month H. felis infected WT and Gli1-/- stomachs.
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Project description:GLI1 is a transcription factor correlated to decreased survival in several cancers. We have identified SMARCA2 as a co-regulator that enhances GLI1-mediated transcriptional activity and functions through the C-terminal transcriptional activation domain of GLI1. Central domains including the ATPase motif of SMARCA2 physically interact with GLI1. Evaluation of DNA density indicates GLI1, like SMARCA2, can increase the DNA accessibility with a preference for sites distal to gene transcription start sites and outside the promoter regions (i.e. enhancers). The putative enhancers where accessibility is decreased by the knock down of GLI1 and SMARCA2 are located cis to genes, such as HHIP, that are regulated by GLI1 and implicated in cancer functions. At the putative enhancer for HHIP, the localization of SMARCA2 is at least partially dependent on GLI1’s presence. Understanding this transcriptional regulation by GLI1 and SMARCA2 through altering chromatin accessibility at enhances can provide additional therapeutic targets for cancers dependent on GLI1.
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Project description:Increased expression of GLI1 is associated with poor prognosis for some breast cancer subtypes. A conditional transgenic GLI1 expressing mouse model, with or without heterozygous deletion of Trp53, was used to generate and study GLI1 induced mammary gland tumours. Tumour tissue was serially orthotopically transplanted for at least 10 generations in NSG mice.
2019-06-30 | E-MTAB-7531 | biostudies-arrayexpress
Project description:We have previously reported human gastrin overexpressing transgenic mice (=INS-GAS mice) and Helicobacter felis (=H.felis) infection synergistically accelerated gastric cancer in mice stomachs. (Wang et al 2000) Using this mouse model, we employed microarray analysis of gene expression profiling to identify gastric cancer-specific genes. Experiment Overall Design: 30 male INS-GAS mice (FVB/N background) were divided into groups: 15 mice were infected with H.felis at the age of 2-3 months and another 15 mice were not infected. 30 male non-transgenic FVB/N mice were also divided into 2 groups: 15 mice were infected with H.felis at the age of 2-3 months and another 15 mice were not infected. All mice were sacrificed after 6 months of H.felis infection, and total RNAs were extracted from whole stomachs. Experiment Overall Design: Histological analysis confirmed all of the stomachs in H.felis infected INS-GAS mice (=INSGAS+Hf) had intra-epithelial gastric cancer, and some of them also had invasion into submucosa, but none of them had distant metastatic lesions. Other 3 control groups had following histology in stomachs. (1) non-transgenic mice with H.felis infection (=FVB+Hf): severe intestinal metaplasia and/or mild dysplasia. (2) INS-GAS mice without infection (=INSGAS wt): severe atrophic gastritis and/or mild intestinal metaplasia (3) non-transgenic mice without infection (=FVB wt): normal stomach. Total RNAs extracted from each mouse in 4 different groups were used for microarray analysis of Affymetrix GeneChip. Experiment Overall Design: Up- or down-regulated genes in INSGAS+Hf group compared with all 3 control groups (FVB+HF, INSGAS wt and FVB wt) may represent gastric cancer-specific genes.
2008-06-13 | E-GEOD-4651 | biostudies-arrayexpress
Project description:GLI1 is a transcription factor correlated to decreased survival in several cancers. We have identified SMARCA2 as a co-regulator that enhances GLI1-mediated transcriptional activity and functions through the C-terminal transcriptional activation domain of GLI1. Central domains including the ATPase motif of SMARCA2 physically interact with GLI1. Evaluation of DNA density indicates GLI1, like SMARCA2, can increase the DNA accessibility with a preference for sites distal to gene transcription start sites and outside the promoter regions (i.e. enhancers). The putative enhancers where accessibility is decreased by the knock down of GLI1 and SMARCA2 are located cis to genes, such as HHIP, that are regulated by GLI1 and implicated in cancer functions. At the putative enhancer for HHIP, the localization of SMARCA2 is at least partially dependent on GLI1’s presence. Understanding this transcriptional regulation by GLI1 and SMARCA2 through altering chromatin accessibility at enhances can provide additional therapeutic targets for cancers dependent on GLI1.
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Project description:The estuarine tapertail anchovy, Coilia nasus, is an anadromous fish that undertakes over a 600-km spawning migration along the Yangtze River of China. They generally cease feeding during this process, but we recently documented that a small proportion of them appear to feed. Research on proteomic responses is essential for understanding the phenomenon of C. nasus feeding. In this study, we used an iTRAQ-based proteomics approach to study the changes in protein expression in response to food intake in C. nasus following voluntary fasting. Coilia nasus in the feeding group (CSI) were fed shrimp or small fish, whereas those in the control group (CSN) were starved. We identified 3279 proteins in the gastric tissue/stomach, of which 279 were significantly differentially expressed. In all, 133 differentially expressed proteins (DEPs) were upregulated and 146 proteins were downregulated in CSI compared with those in CSN C. nasus. In addition to gastric acid secretion caused by gastric distention, a functional analysis suggested that a series of DEPs were involved mainly in the regulation of protein digestion (e.g., carboxypeptidase A1 and chymotrypsin A-like), immune response (e.g., lysozyme and alpha 2-macroglobulin), and nutrition metabolism (e.g., glyceraldehyde 3-phosphate dehydrogenase, glycogenin, long-chain acyl-CoA synthetase, and creatine kinase). Real-time PCR confirmed that the mRNA levels of the DEPs were similar those obtained using iTRAQ. These results indicate that the nutrients obtained through food were effectively utilized by C. nasus, thereby providing energy for swimming, gonadal maturation, primary metabolism, and an enhanced immune function to better resist pathogen interference. This research contributes to the elucidation of nutritional regulation mechanisms of C. nasus to better protect the wild population.
2022-05-25 | PXD033476 | Pride
Project description:We are now trying to elucidate the mechanism of Helicobacter-induced gastritis and gastric cancer. To identify genes involved in these Helicobacter-associated diseases, we infected Helicobacter felis to INS-GAS (insulin-gastrin transgenic) mice (C57BL/6 background) which shows accelerated development of gastritis and gastric cancer. Three infected mice and three uninfected control mice (6 in total) were sacrificed periodically (2, 4, 6, 8 months after the infection), and total RNA was isolated from each stomach. These samples are subjected to gene microarray analysis. Samples were obtained from mouse stomachs at 2, 4, 6, and 8/9 month post infection intervals. Control time points were taken at 0, 2, 4, 6, and 8 months. All samples, 22 in total, were hybridized to the GLYCOv2 array.
2011-02-17 | E-GEOD-27361 | biostudies-arrayexpress
Project description:Purpose: Sox2 expression marks gastric stem and progenitor cells, raising important questions regarding the genes regulated by Sox2 and the role of Sox2 itself during stomach homeostasis and disease. The goal of this study is to determine the function of and the genes regulated by Sox2 in the stomach. Methods: mRNA profiles of Sox2 WT and Sox2 KO gastric glands were generated by RNA-sequencing, in triplicate, using a Illumina HiSeq 2500 instrument, resulting in 36 million single-end 50bp reads per smaple. Sequencing reads were mapped to the mouse reference genome (mm10/GRCm38) using STAR (Dobin et al., 2013). Read counts over transcripts were calculated using HTSeq v.0.6.0 (Anders et al., 2015) based on a current Ensembl annotation file for mm10/GRCm38 (release 75). Results: Sox2 is dispensiable for gastric stem cell self-renewal and epithelial homeostasis, however modulates the expression of cancer and intestinal related genes. mRNA profiles of stomachs from 10 week old Sox2 WT and Sox2 KO mice were generated by sequencing, in triplicate, using a Illumina HiSeq 2500.
2016-08-04 | E-GEOD-83964 | biostudies-arrayexpress
Project description:Background: Helicobacter pylori (H. pylori) infection is a known cause of many digestive diseases, including gastritis, peptic ulcers, and gastric cancer. However, the underlying mechanism(s)by which H. pylori infection triggers these disorders are still not clearly understood. Methods: We have developed an accelerated disease progression mouse model, which leverages mice deficient in the myeloid differentiation primary response 88 gene (Myd88-/-) infected with Helicobacter felis (H. felis) Findings: In this study, we found that H. felis-induced inflammation in Myd88-/- mice progressed to high-grade dysplasia, driven by activation of the type I interferon (IFN-I) signaling pathway and upregulation of its downstream targets, IFN-stimulated genes (ISGs). We also observed enrichment of IFN stimulated-response element (ISRE) motifs in the promoters of upregulated genes, further supporting the involvement of this pathway. In contrast, mice deficient in Toll/interleukin-1 receptor (TIR)-domain-containing adaptor inducing interferon-β (TRIF, TrifLps2) did not progress to severe gastric pathology after H. felis infection, implicating the TRIF signaling pathway in disease pathogenesis and progression. Additionally, analysis of gastric biopsy samples from human gastric cancer patients illustrated that low expression of Myd88 and high expression of Trif were both significantly correlated with poor survival. Interpretation: Our study using an accelerated animal model for gastric cancer and gastric biopsy samples from patients demonstrated that activation of the TRIF-IFN-I signaling pathway promotes Helicobacter-induced disease progression toward severe gastric pathology and gastric cancer development. This represents a potential target for therapeutic intervention, and further exploration may lead to the identification of novel treatment strategies.
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