scholarly journals Differentially Expressed mRNAs and Their Long Noncoding RNA Regulatory Network with Helicobacter pylori-Associated Diseases including Atrophic Gastritis and Gastric Cancer

2020 ◽  
Vol 2020 ◽  
pp. 1-16
Author(s):  
Songyi Liu ◽  
Honghao Yin ◽  
Shuwen Zheng ◽  
Aining Chu ◽  
Yizhi Li ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Atrophic Gastritis ◽  
Regulatory Network ◽  
Noncoding Rna ◽  
Differentially Expressed ◽  
Pathway Enrichment Analysis ◽  
Gastric Diseases ◽  
Associated Diseases ◽  
The Cross

Background. Helicobacter pylori (Hp) infection is the strongest risk factor for gastric cancer (GC). However, the mechanisms of Hp-associated GC remain to be explored. Methods. The gene expression profiling (GSE111762) data were downloaded from the GEO database. Differentially expressed genes (DEGs) between normal samples (NO) and Hp-atrophic gastritis (GA) or Hp-GA and Hp-GC were identified by GEO2R. Gene Ontology and pathway enrichment analysis were performed using the DAVID database. lncRNA-TF-mRNA and ceRNA regulation networks were constructed using Cytoscape. The cross-networks were obtained by overlapping molecules of the above two networks. GSE27411 and GSE116312 datasets were employed for validation. Results. DEGs between NO and Hp-GA are linked to the activity of inward rectifying potassium channels, digestion, etc. DEGs between Hp-GA and Hp-GC were associated with digestion, positive regulation of cell proliferation, etc. According to the lncRNA-TF-mRNA network, 63 lncRNAs, 12 TFs, and 209 mRNAs were involved in Hp-GA while 16 lncRNAs, 11 TFs, and 92 mRNAs were contained in the Hp-GC network. In terms of the ceRNA network, 120 mRNAs, 18 miRNAs, and 27 lncRNAs were shown in Hp-GA while 72 mRNAs, 8 miRNAs, and 1 lncRNA were included in the Hp-GC network. In the cross-network, we found that immune regulation and differentiation regulation were important in the process of NO-GA. Neuroendocrine regulation was mainly related to the process of GA-GC. In the end, we verified that CDX2 plays an important role in the pathological process of NO to Hp-GA. Comparing Hp-GA with Hp-GC, DEGs (FPR1, TFF2, GAST, SST, FUT9, and SHH), TF, and GATA5 were of great significance. Conclusions. We identified the DEGs, and their lncRNA regulatory network of Hp-associated diseases might provide insights into the mechanism between Hp infection and GC. Furthermore, in-depth studies of the molecules might be useful to explore the multistep process of gastric diseases.

scholarly journals The Construction and Analysis of ceRNA Network in H pylori infection atrophic gastritis

2021 ◽  
Author(s):  
Wen-jun BAI ◽  
Jun-wei LIANG ◽  
Xiao-yan WANG
Keyword(s):  
Gastric Cancer ◽  
Atrophic Gastritis ◽  
Signaling Pathway ◽  
Regulatory Network ◽  
Interaction Analysis ◽  
Mapk Signaling ◽  
Functional Enrichment ◽  
Differentially Expressed ◽  
Signal Pathways ◽  
H Pylori

Abstract Background：Chronic atrophic gastritis (CAG) is an established pre-cancerous lesion of intestinal type gastric cancer(GC),H pylori infection is the main pathogenic cause,this study intends to study the pathogenesis of atrophic gastritis(Hp+) from the lncRNA-miRNA-mRNA ceRNA regulatory network, in order to provide the oretical basis and data support for the treatment of atrophic gastritis.Results:GSE111762 downloaded from GEO database was used to analyze the differentially expressed lncRNAs and mRNAs(DEGs).A total of 395 differentially expressed lncRNA (225 upregulated,170 downregulated) and 1093 DEGs ( 674 upregulated, 419 downregulated) are obtained. Through the cross-mapping of miRcode, starBase, Sponescan,miRTarBase and miRBase databases,16 miRNAs were predicted,and the lncRNA-miRNA-mRNA ceRNA regulatory network consisting of 71 IncRNAs,16 miRNAs and 597 mRNAs was constructed.597 DEGs were analyzed by David database for functional enrichment. A total of 250 GO enrichment items were obtained, including 160 BP entries, 48 CC entries and 42 MF entries,29 signal pathways were obtained by enrichment analysis of KEGG pathways, mainly p53 signaling pathway, PI3K-Akt signaling pathway and MAPK signaling pathway. Using Cytoscape plug-in CytoHubba to filter 597 DEGs with "MCC, MNC, Degree" top20 as screening conditions, Eleven key hub targets are obtained from the intersection of jvenn.Protein interaction analysis of key hub targets through Cytoscape plug-in GeneMania, it was found that 87.65% displayed similar co-expression characteristics.Construct ceRNA regulatory network of the key hub targets,11 mRNAs(such as BRCA1, RAD54L),12 miRNAs(such as hsa-miR-340-5p,hsa-miR-182-5p) and 58 lncRNAs(such as PCGEM1,FTX) were predicted. Conclusions:Clarify the complex reticular regulation of atrophicgastritis with multi-targets, multi-pathways and multi-pathways.Which provides a new idea for the study of the mechanism of action of atrophicgastritis (Hp+) and a potential target for its treatment,thus to further early diagnosis and reversal of gastric cancer.

scholarly journals The correlation between lncRNAs and Helicobacter pylori in gastric cancer

2019 ◽  
Vol 77 (9) ◽  
Author(s):  
Narges Dastmalchi ◽  
Seyed Mahdi Banan Khojasteh ◽  
Mirsaed Miri Nargesi ◽  
Reza Safaralizadeh
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Molecular Mechanisms ◽  
Gastrointestinal Diseases ◽  
Mechanisms Of Action ◽  
Molecular Pathways ◽  
Gastric Diseases ◽  
Non Coding Rnas ◽  
H Pylori ◽  
The Relationship

ABSTRACT Helicobacter pylori infection performs a key role in gastric tumorigenesis. Long non-coding RNAs (lncRNAs) have demonstrated a great potential to be regarded as effective malignancy biomarkers for various gastrointestinal diseases including gastric cancer (GC). The present review highlights the relationship between lncRNAs and H. pylori in GC. Several studies have examined not only the involvement of lncRNAs in H. pylori-associated GC progression but also their molecular mechanisms of action. Among the pertinent studies, some have addressed the effects of H. pylori infection on modulatory networks of lncRNAs, while others have evaluated the effects of changes in the expression level of lncRNAs in H. pylori-associated gastric diseases, especially GC. The relationship between lncRNAs and H. pylori was found to be modulated by various molecular pathways.

Prospective Assessment of Helicobacter Pylori Infection and Gastric Pathologies in Sidi Bel Abbes region, Western Algeria

2018 ◽  
Vol 7 (5) ◽  
pp. 217-224
Author(s):  
Zouaouia Chama ◽  
Khedoudj Kanoun ◽  
Fatima Zohra Elkadi ◽  
Kara Turqui Douidi ◽  
Noria Harir ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Histological Study ◽  
Helicobacter Pylori Infection ◽  
University Hospital ◽  
Infection Prevalence ◽  
Gastric Diseases ◽  
Number Of Patients ◽  
H Pylori ◽  
The Impact

Helicobacter pylori infection concerns half of the world’s population, mainly in developing countries. It causes several gastrodudenal pathologies such as gastritis, ulcer and gastric adenocarcinoma. The aim of our study was to determine the prevalence of H.pylori infection and to assess the impact of different epidemiological factors as well as principal gastric diseases associ-ated to this infection. We underwent a prospective study during 18 months (month 2016-month 2017) which implicated 201 symptomatic patients for gastric fiboptic endoscopy at the level of Sidi Bel Abbes University hospital. We collected patients’ biopsies to perform a histological study and H. pylori culture. H. pylori identification was carried out based on bacteriological and biochemical analysis. The middle age of our population was (47.29 ±15.97ans) and the sex-ratio =0,8. The global prevalence of Helicobacter pylori infection is of 61.2% (123/201). This rate, after a statistic analysis, seems to be significantly related to age. It is particularly high especially for patients belonging to age range (20-30)-(51-60) years. The gender did not affect the infection prevalence that is more frequent in the gastritis case. We noticed also that HP infection prevalence was important in SBA the hospital. The range age (20-30)-(51-60) years had the highest prevalence of H. pylori and of gastritis which might be a risky ground of gastric cancer appearance. The ulcer pathology maximal rate concerned the group of 51 to 60 years. Above this age, this rate dropped whereas the number of patients suffering from gastric cancer, which presents an important rate in our study, increase for the group of 61-70 years.

scholarly journals Helicobacter Pylori Induce Gastric Upset

2021 ◽  
pp. 1-1
Author(s):  
Hazim Abdul Rahman Alhit
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Serum Antibody ◽  
Endoscopic Biopsy ◽  
Helicobacter Pylori Infection ◽  
Gastric Epithelium ◽  
Gastric Diseases ◽  
Heterogeneous Distribution ◽  
Cytotoxin Associated Gene A ◽  
H Pylori

Editorial: Helicobacter pylori is a micro-aerophilic, helical-form gramnegative aggressive bacteria. Accordingly, the idiom “Helico” intimates its helical appearance, “bacter” symbolizes bacteria, while “pylori” denotes stomach due to the first and common site of this bacteria living. Further, Marshall B. and Warren R. observed and described it in 1982. Then, the followed investigators studied this bacterium in detail with its consequences and complexities [1]. Gastric upset (Indigestion), dyspepsia: means impaired gastric digestion. Accordingly, the patient complains of upper abdominal pain, heartburn, belching, nausea, even feeling earlier gastric fullness than expected while eating. Furthermore, there are many causes of indigestion like gastroesophageal reflux disease, ulcer disease, gastritis, and even gastric cancer. Hence, unexplained recent onset dyspepsia in older people may need additional examinations. Moreover, one of the common causes is Helicobacter pylori infection, which needs laboratory and endoscopic examination [2]. Argument Many theories investigated the etiology and pathogenesis of Helicobacter pylori infection, concerning chronic or acute gastritis. Hence, gastric upset is the main presentation of both types of gastritis. Evidences The genotype is valuable in determining the dominant Helicobacter pylori strains as the isolates were different genetically plus heterogeneous distribution. Accordingly, the vac and cag markers operate a significant function in defining clinical consequences. These virulence agents are present in a subset of Helicobacter pylori strains isolates like cagA, iceA, vacA, and ureC. Moreover, the cagA causes cytotoxins induction by the gastric epithelial cell as Interleukin 8 [3]. The molecular intercommunication researches exhibit that the act of acarus calamus in hindering biofilm formation in Helicobacter pylori is due to the inhibitory impact of phytobio-active component, β-sitosterol, on the quorum sensing molecules-ToxB, PhnB, DnaA, plus Sip. Consequently, this opinion may suggest the molecular mechanism of Helicobacter pylori in producing the acidrelated complaints and gives a clue to a new therapy [4]. Helicobacter pylori infection causes lncRNA risk impression linked to H. pylori in gastric cancer patients and can prognosticate the prediction of these patients [5]. There was a close relationship between raised serum IgE levels in Helicobacter pylori infected patients [6]. Counterargument The laboratory investigations of Helicobacter pylori infection depend on several factors like the fluctuations of serum antibody titers in a time series, the antigene detection in stool tests, the false-positive results of lab tests, or the manner of endoscopic biopsy collection. Furthermore, other factors like the variations in Cytotoxin-Associated Gene A (CagA) in East Asian patients. Moreover, the gastric nodularity or atrophy, the patient’s age, the severity of the gastric mucosal infection are causes of variations in Helicobacter pylori detection at the time of the investigation [7]. Refutation The significant markers of H. pylori, the presence of the vacuolating cytotoxin (vacA), the cytotoxin-associated gene A (cagA), which induced by the direct communication with gastric epithelium factor antigen (iceA gene), and the presence of urease C gene (ureC). Consequently, all these factors play the principal factors in deciding the gastric consequences of Helicobacter infections. Conclusion Helicobacter pylori induce gastric upset by several mechanisms to form numerous Gastric diseases.

scholarly journals Cross-sectional study of human coding- and non-coding RNAs in progressive stages of Helicobacter pylori infection

2020 ◽  
Vol 7 (1) ◽  
Author(s):  
Sergio Lario ◽  
María J. Ramírez-Lázaro ◽  
Aintzane González-Lahera ◽  
José L. Lavín ◽  
Maria Vila-Casadesús ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Expression Profiles ◽  
Gastric Carcinogenesis ◽  
Individual Response ◽  
Peptic Ulcers ◽  
Gastric Diseases ◽  
Sequence Of Events ◽  
Non Coding Rnas ◽  
H Pylori

Abstract Helicobacter pylori infects 4.4 billion individuals worldwide and is considered the most important etiologic agent for peptic ulcers and gastric cancer. Individual response to H. pylori infection is complex and depends on complex interactions between host and environmental factors. The pathway towards gastric cancer is a sequence of events known as Correa’s model of gastric carcinogenesis, a stepwise inflammatory process from normal mucosa to chronic-active gastritis, atrophy, metaplasia and gastric adenocarcinoma. This study examines gastric clinical specimens representing different steps of the Correa pathway with the aim of identifying the expression profiles of coding- and non-coding RNAs that may have a role in Correa’s model of gastric carcinogenesis. We screened for differentially expressed genes in gastric biopsies by employing RNAseq, microarrays and qRT-PCR. Here we provide a detailed description of the experiments, methods and results generated. The datasets may help other scientists and clinicians to find new clues to the pathogenesis of H. pylori and the mechanisms of progression of the infection to more severe gastric diseases. Data is available via ArrayExpress.

scholarly journals Helicobacter pylori and Epstein–Barr Virus Infection in Gastric Diseases: Correlation with IL-10 and IL1RN Polymorphism

2019 ◽  
Vol 2019 ◽  
pp. 1-8 ◽  
Author(s):  
Fasciana Teresa ◽  
Nicola Serra ◽  
Giuseppina Capra ◽  
Chiara Mascarella ◽  
Cesare Gagliardi ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Chronic Gastritis ◽  
Epstein Barr Virus ◽  
Normal Gastric Mucosa ◽  
Gastric Diseases ◽  
Barr Virus ◽  
Genes Encoding ◽  
Epstein Barr

Introduction. Helicobacter pylori and Epstein–Barr virus (EBV) infection have recently been shown to be associated with gastric diseases. Polymorphisms in genes encoding cytokines such as interleukin 10 (IL-10) and interleukin 1 Receptor (IL-1RN) influence cytokine secretion levels and appear to contribute to the risk of developing gastroduodenal diseases. To our knowledge, this is the first preliminary study to address the association of coinfection with H. pylori and EBV and their correlation with genetic predisposition in the development of gastric diseases. Methods. Gastric biopsy samples of 96 patients with different gastric diseases were used. Results. Our results showed that the rate of coinfection was higher in patients with gastric cancer than in patients with normal gastric mucosa, active chronic gastritis, and MALT lymphoma. As regards the characterization of H. pilory strains, the polymorphism s1m1i1 of vacA gene was more frequent in patients with MALT Lymphoma in comparison to others, while the polymorphism s2m2i2 was most frequent in patients with normal gastric mucosa. In addition, patients who tested positive for the cagA gene were more frequently those affected with gastric cancer than those with inactive chronic gastritis. Similarly, the patients with oipA gene ON were more frequently those with gastric cancer than those with inactive chronic gastritis. Conclusion. According to our analysis, there was no correlation between coinfection and polymorphisms in genes encoding IL-10 and IL-1RN. We conclude that various factors can be involved in the development of gastric diseases.

scholarly journals Identification of Potential Biomarkers and Biological Pathways in Juvenile Dermatomyositis Based on miRNA-mRNA Network

2019 ◽  
Vol 2019 ◽  
pp. 1-9 ◽  
Author(s):  
Cheng-Cheng Qiu ◽  
Qi-Sheng Su ◽  
Shang-Yong Zhu ◽  
Ruo-Chuan Liu
Keyword(s):  
Regulatory Network ◽  
Messenger Rna ◽  
Target Genes ◽  
Juvenile Dermatomyositis ◽  
Type I Diabetes ◽  
Differentially Expressed ◽  
Pathway Enrichment Analysis ◽  
Type I ◽  
Ppi Network ◽  
Potential Biomarkers

Objective. The aim of this study is to explore the potential pathogenesis of juvenile dermatomyositis by bioinformatics analysis of gene chips, which would screen the hub genes, identify potential biomarkers, and reveal the development mechanism of juvenile dermatomyositis. Material and Methods. We retrieved juvenile dermatomyositis’s original expression microarray data of message RNAs (mRNAs) and microRNAs (miRNAs) from NCBI’s Gene Expression Omnibus database (GEO, http://www.ncbi.nlm.nih.gov/geo/); through the R package of limma in Bioconductor, we can screen the differentially expressed miRNAs and mRNAs, and then we further analyzed the predicted target genes by the methods such as Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis and miRNA-mRNA regulatory network construction and protein-protein interaction (PPI) network using Cytoscape 3.6.1. Results. Compared with normal juvenile skin tissues, 6 upregulated microRNAs and 5 downregulated microRNAs were identified from 166 downregulated microRNAs and 58 upregulated microRNAs in juvenile dermatomyositis tissues. The enrichment pathways of differentially expressed microRNAs include cell adhesion molecules (CAMs), autoimmune thyroid disease, Type I diabetes mellitus, antigen and presentation, viral myocardium, graft-versus-host disease, and Kaposi sarcoma-associated herpes virus infection. By screening of microRNA-messenger RNA regulatory network and construction of PPI network map, three target miRNAs were identified, namely, miR-193b, miR-199b-5p, and miR-665. Conclusion. We identified mir-193b, mir-199b-5p, and mir-6653 target miRNAs by exploring the miRNA-mRNA regulation network mechanism related to the pathogenesis of juvenile dermatomyositis, which will be of great significance for further study on the pathogenesis and targeted therapy of juvenile dermatomyositis.

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