CircMAN1A2 is upregulated by Helicobacter pylori and promotes development of gastric cancer
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA761426 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR15744321_1.fastq.gz | Fastqsanger.gz | |||
| SRR15744321_2.fastq.gz | Fastqsanger.gz | |||
| SRR15744322_1.fastq.gz | Fastqsanger.gz | |||
| SRR15744322_2.fastq.gz | Fastqsanger.gz | |||
| SRR15744323_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 12 |
Similar Datasets
Project description:In this study, we treated the gastric cancer cell line AGS with PBS and Helicobacter pylori to perform RNA-seq analysis. A total of 18,308 different circRNA candidates were obtained in the experiment.Compared with the control, 101 significantly differentially expressed circRNAs were identified in the AGS cells infected with H. pylori, including 84 upregulated circRNAs and 17 downregulated circRNAs.Then, circMAN1A2 with the most significant expression difference was selected according to the sequencing results to study the epigenetic mechanism of H. pylori-induced gastric carcinogenesis.
2021-09-09 | GSE183628 | GEO
Project description:Helicobacter pylori is the primary cause of gastric cancer and there is a need to discover new molecular targets for therapeutic intervention in H. pylori disease progression. We have previously shown that spermine oxidase (SMOX), the enzyme that catabolizes the back-conversion of the polyamine spermine to spermidine, is upregulated during infection and is associated with increased cancer risk in humans. We sought to determine the direct role of SMOX in gastric carcinogenesis during H. pylori infection. In this study, we demonstrate that transgenic FVB/N insulin-gastrin (INS-GAS) mice that develop gastric carcinoma with H. pylori infection were protected from cancer development with Smox deletion. RNA sequencing revealed that genes associated with the immune system and cancer were downregulated in the infected Smox–/– mice. Furthermore, there was a decrease in cell proliferation and DNA damage in infected Smox–/– animals. There was significant generation of adducts of the highly reactive electrophile acrolein, a byproduct of SMOX activity, in tissues from H. pylori-infected WT mice and humans. Genetic deletion of Smox or chemical inhibition of SMOX in murine organoids and human gastric epithelial cells and organoids, respectively, significantly reduced generation of acrolein induced by H. pylori. Furthermore, acrolein induced DNA damage in gastric epithelial cells, which was ablated with the electrophile scavenger 2-hydroxybenzylamine (2-HOBA). Infected 2-HOBA treated INS-GAS WT mice with reduced gastric carcinoma had attenuated gastric acrolein adduct formation. These findings implicate SMOX and acrolein in H. pylori-induced carcinogenesis in gastric epithelial cells, thus indicating potential therapeutic targets.
2025-02-05 | GSE266944 | GEO
Project description:Helicobacter pylori (H. pylori) infection is characterized as progressive processes of bacterial persistence and chronic gastritis with features of infiltration of mononuclear cells more than granulocytes in gastric mucosa. Angiopoietin-like 4 (ANGPTL4) is considered a double-edged sword in inflammation-associated diseases, but its function and clinical relevance in H. pylori-associated pathology is unknown. Here we demonstrate both pro-colonization and pro-inflammation roles of ANGPTL4 in H. pylori infection. Increased ANGPTL4 in the infected gastric mucosa was produced from gastric epithelial cells (GECs) synergistically induced by H. pylori and IL-17A in a cagA-dependent manner. Human gastric ANGPTL4 correlated with H. pylori colonization and the severity of gastritis, and mouse ANGPTL4 from non-bone marrow-derived cells promoted bacteria colonization and inflammation. Importantly, H. pylori colonization and inflammation were attenuated in Il17a-/-, Angptl4-/-, Il17a-/-Angptl4-/- mice. Mechanistically, ANGPTL4 bound to integrin αV (ITGAV) on GECs to suppress CXCL1 production by inhibiting ERK, leading to decreased gastric influx of neutrophils, thereby promoting H. pylori colonization; ANGPTL4 also bound to ITGAV on monocytes to promote CCL5 production by activating PI3K-AKT-NF-κB, resulting in increased gastric influx of regulatory CD4+ T cells (Tregs) via CCL5-CCR4-dependent migration. In turn, ANGPTL4 induced Treg proliferation through binding to ITGAV to activate PI3K-AKT-NF-κB, promoting H. pylori-associated gastritis. Overall, we propose a model in which ANGPTL4 collectively ensures H. pylori persistence and promotes gastritis. Efforts to inhibit ANGPTL4-associated pathway may prove valuable strategies in treating H. pylori infection.
2024-05-15 | GSE266891 | GEO
Project description:Helicobacter pylori (H. pylori) infection is the most common risk factor for gastric cancer (GC). The effect of the antioxidase manganese superoxide dismutase (SOD2) in gastric tumorigenesis remains unclear. We explored the molecular and mechanical links between H. pylori, inflammation, and SOD2 in GC. We found SOD2 was upregulated in GC. GC patients with high SOD2 expression showed worse overall survival. H. pylori infection promoted SOD2 expression by transcriptionally activating the NF-κB signaling pathway. Knockdown of SOD2 led to increased levels of reactive oxygen species and oxidative stress in response to H. pylori infection. Our research demonstrated that SOD2 can serve as an inhibitor of ferroptosis by activating AKT, stabilizing GPX4 protein, which subsequently induces 5-fluorouracil resistance. These findings reveal a mechanism whereby H. pylori can promote gastric carcinogenesis by activating the NF-κB/SOD2/AKT/GPX4 pathway, leading to the inhibition of ferroptosis. This may provide a promising therapeutic target for GC.
2024-10-14 | GSE278591 | GEO
Project description:Helicobacter pylori are gram-negative bacteria that colonize the human stomach and are the major etiological factor in gastric carcinoma development. The aim of this work was to evaluate changes in gene expression in gastric cells induced by H. pylori.
2016-03-01 | GSE70394 | GEO
Project description:Helicobacter pylori (H. pylori) infects nearly half of the global population. H. pylori infection is associated with various gastric diseases and is a recognized causative factor for gastric cancer. The mechanisms underlying the persistent colonization of H. pylori and its role in the development and progression of gastritis-associated carcinogenesis remain unclear. To investigate the pathogenic mechanisms of H. pylori infection, we performed RNA sequencing (RNA-seq) on H. pylori-infected gastric epithelial cells and analyzed the gene expression patterns induced by H. pylori infection, aiming to provide critical insights for understanding its disease-driving pathways.
2025-04-29 | GSE295523 | GEO
Project description:Helicobacter pylori (H. pylori) is a human pathogen that infects almost half of the world’s population. Infection with H. pylori is frequently associated with chronic gastritis and can even lead to gastric and duodenal ulcers and gastric cancer. Although the persistent colonization of H. pylori and the development of H. pylori-associated gastritis remain poorly understood, it is believed that, in gastric mucosa, the modulated gastric epithelial cells (GECs) by H. pylori are key contributors. We used microarrays to detail the global programme of gene expression in Helicobacter pylori infected-gastric epithelial cell line AGS cells and identified up-regulated genes induced by Helicobacter pylori infection.
2024-04-18 | GSE264263 | GEO
Project description:Helicobacter pylori clinical isolates can establish themselves in gastric epithelial stem cells and this interaction may have implications for gastric tumorigenesis. Mouse gastric epithelial progenitor cells (mGEPs) and non-progenitor gastric epithelial cells (npGECs) were infected for 24hrs with Helicobacter pylori clinical isolates Kx1 and Kx2. Kx1 was isolated from a patient with chronic atrophic gastritis (ChAG) and Kx2 from the same patient 4 years later, when he progressed to gastric adenocarcinoma. Keywords: RNA Expression Array
2008-02-22 | GSE10262 | GEO
Project description:Helicobacter pylori clinical isolates can establish themselves in gastric epithelial stem cells and this interaction may have implications for gastric tumorigenesis. Mouse gastric epithelial progenitor cells (mGEPs) were infected for 24hrs with Helicobacter pylori clinical isolates Kx1 and Kx2. Kx1 and Kx2 were also grown in cell media in the absence of cells. Kx1 was isolated from a patient with chronic atrophic gastritis (ChAG) and Kx2 from the same patient 4 years later, when he progressed to gastric adenocarcinoma. Keywords: RNA Expression Array
2008-02-22 | GSE10261 | GEO
Project description:Helicobacter pylori are gram-negative bacteria that colonize the human stomach and are the major etiological factor in gastric carcinoma development. The aim of this work was to evaluate changes in gene expression in gastric cells induced by H. pylori. The human gastric carcinoma-derived cell line AGS was infected with H. pylori strain 60190 (ATCC 49503) for 24 hours. RNA was extracted from three independent experiments.
2016-03-01 | E-GEOD-70394 | biostudies-arrayexpress