Lnc-PLCB1 is stabilized by METTL14 induced m6A modification and inhibits Helicobacter pylori mediated gastric cancer by degrading DDX21
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE231672 | GEO | 2023/10/30
REPOSITORIES: GEO
Similar Datasets
Project description:With the colonization of Helicobacter Pylori (H.pylori) in the human stomach, a large amount of Helicobacter Pylori (H.pylori)colonized into the stomach disintegrates and releases a large number plenty of toxic proteins and other bacterial structure components. TollToll-like receptors (TLRs) in gastric epithelial cells which sensitive to the components of bacteria lysate around the microenvironment attach them and activite innate immune and pro-inflammatory response once contact with antigen. The consequences after long-term stimulation of H.pylori lysate in gastric epithelial cells has not been reported . To investigate the effects of H.pylori lysate on TLRs expression and inflammatory cytokines level during long-term stimulation of gastric epithelial cells and clarify the potential mechanismHence, we detected TLRs mRNA level and inflammatory cytokines expression in GES-1 cells co-culture with lysate from 1 to 30 generations. The sensitivity to H.pylori or H.pylori lysate in GES-1 cells were also monitored. We also explored whether LPS was the main factors contributing to this change. Mongolian gerbils were used to replicate H.pylori infection animal model. After transcriptome sequencing，A TLR2/6 heterodimers agonist Pam2CSK4 and a highly selective inhibitor of PI3K LY294002 were used to clarify the TLR6 signaling pathways. In a conclusion, we discovered that the sensitivity of TLRs in human gastric epithelial cells decreased while after long-time co-culture with H.pylori lysate. Human gastric epithelial cells shows tolerance to H.pylori lysate in TLRs and inflammatory cytokines level. decreased the high level of TLRs and inflammatory cytokines after stimulating GES-1 cells with H.pylori lysate for a short-term. And Tthis process may works through the TLR6/PI3K/NF-κKB axis.
2021-04-18 | GSE149092 | GEO
Project description:Unbiased de-novo identification of biomarkers for H.pylori associated gastric cancer; Microarrays, representing 242 seroreactive H.pylori proteins, were generated by spotting of the respective gene constructs and cell-free on-chip expression. Antibody levels to these proteins were measured by application of sera from non-cardia gastric cancer patients and their matched controls. Possible new biomarkers, associated with gastric cancer, were evaluated by unadjusted conditional regression.
2020-09-14 | E-MTAB-9534 | biostudies-arrayexpress
Project description:Research on lncRNAs expression profiles in human interactions with Helicobacter pylori (H.pylori) is rare reported. We used HTA2.0 to investigate the expression changes of lncRNAs and mRNAs in human gastric epithelial cells (GES-1 cell line) infected with or without H.pylori infection. Our study provided a preliminary exploration of lncRNAs expression profiles in H.pylori-infected cell models by microarray. A subset of aberrantly expressed lncRNAs was verified by qRT-PCR. These dysregulated lncRNAs might contribute to the pathological processes during H.pylori infection.
2015-11-03 | GSE74577 | GEO
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 (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:Research on lncRNAs expression profiles in human interactions with Helicobacter pylori (H.pylori) is rare reported. We used HTA2.0 to investigate the expression changes of lncRNAs and mRNAs in human gastric epithelial cells (GES-1 cell line) infected with or without H.pylori infection. Our study provided a preliminary exploration of lncRNAs expression profiles in H.pylori-infected cell models by microarray. A subset of aberrantly expressed lncRNAs was verified by qRT-PCR. These dysregulated lncRNAs might contribute to the pathological processes during H.pylori infection. We infected GES-1 cells with H.pylori as experimental groups,and cells without H.pylori infection were regarded as control groups. After 24hr-infection, cells of each group were selected for total RNA extraction and hybridization on Affymetrix HTA2.0 arrays. The aberrant expression profiles of lncRNAs and mRNAs were explored by microarray analysis between experimental and control groups.
2015-11-03 | E-GEOD-74577 | biostudies-arrayexpress
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
Project description:The aim of this study was to identify and assess the utility of miRNAs as diagnostic surrogate markers for H.pylori infection. For this purpose, we analyzed the miRNA expression profile by microarrays in the antral mucosa of well characterized dyspeptic patients and then applied the most significant set of miRNAs to an independent validation group. Our results shows that a set of miRNAs are deregulated during chronic gastric inflammation and that this set may be may be useful as a surrogate marker for determining the presence of H.pylori.
2012-09-01 | GSE32174 | GEO
Project description:Helicobacter pylori (H.pylori) infection is a significant risk factor for gastric cancer (GC) development. A growing body of evidence suggests a causal link between infection with H.pylori and increased DNA breakage in the host cells. While several mechanisms have been proposed for this damage, their relative impact on the overall bacterial genotoxicity is unknown. Moreover, the link between the formation of DNA damage following infection and the emergence of cancerous structural variants (SV) in the genome of infected cells remained unexplored. To resolve these gaps, we constructed high-resolution map of genomic H.pylori-induced recurrent break sites. Our data indicated that these sites are ubiquitous across cell types, localized at replication-related fragile sites, and their breakage is dependent on replication. Consistent with that, we found that H.pylori inflicts nucleotide depletion, and that rescuing the nucleotide pool largely reduced H.pylori-induced DNA breaks. Intriguingly, we found that this genotoxic mechanism operates independently of the H.pylori virulence factor, CagA, which was previously implicated in increasing DNA damage by downregulating the DNA damage response. Finally, we show that sites of recurrent H.pylori-mediated breaks coincide with chromosomal deletions observed in patients with intestinal-type GC, and that this link potentially elucidates the persistent transcriptional alterations observed in cancer driver genes. These findings establish the link between H.pylori genotoxicity, and its oncogenic potential.
2024-02-15 | GSE245644 | GEO
Project description:H. pylori infection of human gastric epithelial cells (GEC) represses H,K-ATPase alpha subunit (HK-alpha) gene transcription through NF-Kappa B p50 homodimer binding to HK-alpha promoter. The bacterial cagA and slt gene products have been implicated in HK-alpha repression, which facilitates gastric H. pylori colonization and may underlie transient clinical hypochlorhydria. We hypothesized that H. pylori also regulates H,K-ATPase expression post-transcriptionally by micro-RNA interaction with HK-alpha mRNA. Our microarray experiment examined the effect of infection by wildtype H. pylori infection or a delta-cagA H. pylori mutant on miRNA expression of human gastric cells (AGS). Our results indicate that H. pylori infection up-regulates GEC miRNAs that target the HK-alpha 3' UTR and block translation, and that CagA activity is implicated in the miRNA up-regulation. Three types of samples were generated for microarray analysis: 1) AGS cells infected with wildtype H. pylori; 2) AGS cells infected with cagA-deficient H. pylori; 3) a mock-infected sample, prepared as a control by combining total RNA from uninfected AGS cells with total RNA from wildtype H. pylori, with relative eukaryotic and prokaryotic RNA amounts matching those observed in infected samples, based on proportional ribosomal peak heights quantified by Bioanalyzer. Three experimental replicates were generated for each type of treatment.
2016-01-18 | E-GEOD-51306 | biostudies-arrayexpress