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Lnc-PLCB1 is stabilized by METTL14 induced m6A modification and inhibits Helicobacter pylori mediated gastric cancer by degrading DDX21

ABSTRACT: To determine the role of m6A modification in H.pylori-mediated gastric cancer, we performed RNA methylation immunoprecipitation sequencing (MeRIP-seq) after infecting gastric cancer cell line AGS with H. pylori standard strain Hp26695 at MOI=100 for 12h. The sequencing results include three parts: mRNA, lncRNA, and circRNA.

ORGANISM(S): Homo sapiens

PROVIDER: GSE231672 | GEO | 2023/10/30

REPOSITORIES: GEO

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lnc-PLCB1 is stabilized by METTL14 induced m6A modification and inhibits Helicobacter pylori mediated gastric cancer by degrading DDX21

Project description:lnc-PLCB1 is stabilized by METTL14 induced m6A modification and inhibits Helicobacter pylori mediated gastric cancer by degrading DDX21

| PRJNA967277 | ENA

Transcriptome expression changes in human gastric epithelial cells co-cultured with Helicobacter pylori lysate of different generations.

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

Potential mechanisms by which Jiawei Lianpu Yin inhibits Helicobacter pylori colonization and alleviates gastric mucosal inflammation and damage: Integrated transcriptomics, network pharmacology, and experimental validation

Project description:Ethnopharmacological relevance: Helicobacter pylori (H.pylori) infection is the leading cause of gastric mucosal damage and inflammation, and persistent infection is one of the major risk factors for gastric cancer. Eradication of H.pylori remains a clinical challenge, and therefore, it is urgently necessary to identify more drugs that can interfere with H.pylori colonization and promote its clearance. Jiawei Lianpu Yin (JWLPY) is a compound formula composed of natural drugs used to treat gastric diseases associated with H.pylori infection. However, the underlying mechanisms of its action are still unclear. Aim of the study: The aim of this study was to investigate whether JWLPY can inhibits H.pylori colonization and alleviates gastric mucosal inflammation and damage and to explore its mechanism of action. Materials and METHODS: The effects of JWLPY on Helicobacter pylori and gastric mucosa injury were studied by using Helicobacter pylori induced gastritis model in rats. Transcriptomics, network pharmacology and bioinformatics were used to determine the mechanism of JWLPY Results: JWLPY inhibited the aggregation of inflammatory cells and preserved the integrity of the mucosal barrier, reducing autophagy and apoptosis in gastric mucosal epithelial cells. Network pharmacology and transcriptomics analysis revealed that JWLPY promotes the assembly and synthesis of MUC5AC in the endoplasmic reticulum by activating the IRE1-XBP1 signaling pathway, which enhances the process of protein assembly in the endoplasmic reticulum, thereby inhibiting H.pylori colonization in the gastric mucosa. Conclusion: This study is the first to demonstrate that JWLPY inhibits H.pylori colonization in the gastric mucosa, alleviates gastric inflammation and damage, and is a potential drug for the treatment of H.pylori -related gastritis.

2025-04-03 | GSE293658 | GEO

Identification of gastric cancer associated serum antibodies using Helicobacter pylori antigen microarrays

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

LncRNA and mRNA expression profiles from human GES-1 cells in response to Helicobacter pylori infection

2015-11-03 | GSE74577 | GEO

Expression data from Helicobacter positive and negative human gastritis samples

Project description:The whole-genome oligonucleotide microarray analysis gives an opportunity for studying the unidentified gene expression background of the idiopathic and H.pylori related gastric erosive alterations. Using microarrays we compared the whole genome gene expression profile of HP+ and HP- gastric erosions and normal adjacent mucosa to explain the possible role and response to HP infection and to get morphology related mRNA expression patterns. Keywords: whole genomic expression

2008-06-04 | GSE5081 | GEO

LncRNA and mRNA expression profiles from human GES-1 cells in response to Helicobacter pylori infection

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

Helicobacter pylori infection induces DNA breaks at replication-coupled fragile sites by inducing dNTP depletion in CagA-independent manner

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

microRNA profiling in duodenal ulcer disease caused by Helicobacter pylori infection in a Western population.

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

CircMAN1A2 is upregulated by Helicobacter pylori and promotes development of gastric cancer

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

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