scholarly journals Function of Non-coding RNA in Helicobacter pylori-Infected Gastric Cancer

2021 ◽  
Vol 8 ◽  
Author(s):  
Chao Wang ◽  
Yiyang Hu ◽  
Huan Yang ◽  
Sumin Wang ◽  
Bo Zhou ◽  
...  

Gastric cancer is a common malignant tumor of the digestive system. Its occurrence and development are the result of a combination of genetic, environmental, and microbial factors. Helicobacter pylori infection is a chronic infection that is closely related to the occurrence of gastric tumorigenesis. Non-coding RNA has been demonstrated to play a very important role in the organism, exerting a prominent role in the carcinogenesis, proliferation, apoptosis, invasion, metastasis, and chemoresistance of tumor progression. H. pylori infection affects the expression of non-coding RNA at multiple levels such as genetic polymorphisms and signaling pathways, thereby promoting or inhibiting tumor progression or chemoresistance. This paper mainly introduces the relationship between H. pylori-infected gastric cancer and non-coding RNA, providing a new perspective for gastric cancer treatment.

2019 ◽  
Vol 77 (9) ◽  
Author(s):  
Narges Dastmalchi ◽  
Seyed Mahdi Banan Khojasteh ◽  
Mirsaed Miri Nargesi ◽  
Reza Safaralizadeh

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.


2019 ◽  
Vol 16 (1) ◽  
Author(s):  
Yifeng Zhang ◽  
Jin Yan ◽  
Chao Li ◽  
Xiaoyong Wang ◽  
Yu Dong ◽  
...  

Abstract Background The aim of this study was to investigate the role of long non-coding RNA (lncRNA) H19 in gastric cancer (GC) with Helicobacter pylori (H. pylori). Methods H19 expression in peripheral blood from H. pylori+/− GC patients and healthy donors (control) as well as in GC tissues and cells were detected by qRT-PCR. Cell proliferation was evaluated by CCK-8 assay. Cell migration and invasion were evaluated by Transwell assay. The levels of pro-inflammatory cytokines were determined by ELISA. The protein levels of IκBα, p-IκBα and p65 were determined by western blotting. Results H19 expression was upregulated in H. pylori-infected GC tissues and cells. Furthermore, H. pylori promoted GC cell viability, migration, invasion and inflammatory response. Moreover, H19 overexpression promoted the proliferation, migration and invasion of H. pylori-infected GC cells via enhancing NF-κB-induced inflammation. Conclusions LncRNA H19 promotes H. pylori-induced GC cell growth via enhancing NF-κB-induced inflammation.


2021 ◽  
Vol 6 (1) ◽  
pp. 53-57
Author(s):  
Miluska Castillo ◽  
Luis A. Bernabe ◽  
Carlos A. Castaneda ◽  
Nancy Suarez ◽  
Fernando Barreda ◽  
...  

Objective: The aim of this study was to determine the relationship between Helicobacter pylori (H. pylori) infection in relatives and patients with gastric cancer (GC).Methods: H. pylori infection was evaluated by the breath urease test in 171 relatives and by qPCR technique in gastric tissue of 61 patients (n=45 for GC and n=16 for non-GC). Results: There were included 137 relatives of GC patients and 34 of non-GC. The median age of the relatives of patients with a gastric tissue sample was 39 years (10-86). Infection was found in 60.2% (n=103) relatives. There were no higher H. pylori infection rates in relatives of patients with gastric cancer (62% vs 62.9%, p=0.33), H. pylori infection (60% vs 60%, p=0.96), or metaplasia (58.8% vs 61.8%, p=0.71). Conclusion: The prevalence of infection in relatives of GC patients is high in our population but not associated with H. pylori presence in the paired case.


2003 ◽  
Vol 17 (suppl b) ◽  
pp. 18B-20B ◽  
Author(s):  
Jia-Qing Huang ◽  
Richard H Hunt

The relationship betweenHelicobacter pyloriinfection and the risk of gastric cancer has been well established in the last decade. Four metaanalyses have found that the infection increases the risk of noncardia gastric cancer by 2- to 6-fold compared with noninfected control populations. However, the role ofcagAstrains ofH pyloriin relation to gastric cancer has not been evaluated systematically. We undertook a meta-analysis of epidemiological studies examining the relationship between infection withcagA-positive strains ofH pyloriand the risk of gastric cancer, and found that patients who are seropositive forcagAstrains ofH pyloriare at an increased risk for developing noncardia gastric cancer compared with those withH pyloriinfection alone. Therefore, searching forcagA-positive strains ofH pylorimay help identify populations at a greater risk for developing gastric cancer.


2021 ◽  
Author(s):  
Yuka Hirashita ◽  
Masahide Fukuda ◽  
Masaaki Kodama ◽  
Yoshiyuki Tsukamoto ◽  
Tadayoshi Okimoto ◽  
...  

Abstract Background Although eradication therapy for chronic Helicobacter pylori reduces the risk of gastric cancer (GC), its effectiveness is incomplete. Therefore, it is critically important to identify those patients who remain at high risk after H. pylori eradication therapy. Accumulation of protein methylation is strongly implicated in cancer, and a recent study showed that dimethylation of eEF1A lysine 55 (eEF1AK55me2) promotes carcinogenesis in vivo. We aimed to investigate the relationship between eEF1A dimethylation and H. pylori status in gastric mucosa and to reveal potential downstream molecules of eEF1A dimethylation in H. pylori-eradicated mucosa. Methods Records of 115 patients (11 H. pylori-negative, 29 H. pylori-positive, 75 post-eradication patients) who underwent upper gastrointestinal endoscopy were retrospectively reviewed. The eEF1A dimethyl level was evaluated in each functional cell type of gastric mucosa by immunofluorescent staining. We also investigated the relationship between eEF1AK55me2 downregulation by CRISPR/Cas9-mediated deletion of Mettl13, which is known as a dimethyltransferase of eEF1AK55me2. Results The level of eEF1A dimethylation significantly increased in the surface and basal areas of H. pylori-positive mucosa compared with -negative mucosa (surface, p=0.0031; basal, p<0.0001). The eEF1A dimethyl levels in the surface area were significantly reduced by eradication therapy (p=0.005), but those in the basal area were maintained even after eradication therapy. Multivariate analysis revealed that high dimethylation of eEF1A in the basal area of the mucosa was the independent factor related to GC incidence (odds ratio=3.6611, 95% confidence interval=1.0350–12.949, p=0.0441). We also showed the relationship between eEF1A dimethylation and expressions of reprogramming factors Oct4 and Nanog by immunohistochemistry and in vitro genome editing experiments. Conclusions The results indicated that H. pylori infection potently induced eEF1A dimethylation in gastric mucosa. The accumulation of dimethyl-eEF1A in the basal area of the mucosa might contribute to GC risk via regulation of reprograming factors in H. pylori-eradicated gastric mucosa.


2020 ◽  
Author(s):  
Masoud Keikha ◽  
Mohsen Karbalaei

Abstract Background: Helicobacter pylori (H. pylori) is one of the most well-known risk factors for getting the gastric cancer disease. In recent studies, the relationship between its virulence factors, specially CagA (cytotoxin‐associated gene A) toxin and development into the gastrointestinal diseases is taken into consideration. According to review of literature, despite the presence of four motifs A, B, C, and D in CagA toxin, two motifs C and D are more associated with gastrointestinal complications in patients who are infected by H. pylori. Methods: In the present study, we researched about theses ambiguities using a comprehensive meta-analysis study. In this study, we assessed the information of 1762 Iranian patients for potential relationship between all genotypes of cagA gene and gastrointestinal diseases.Results: According to statistical analysis, the abundance of cagA genotypes AB, ABC, ABCC, ABCCC, and ABD in Iranian population is 5.52%, 80.18%, 22.81%, 2.76%, and 0% respectively. In addition, it was determined that there is a significant relationship between cagA genotypes ABCC and ABCCC on the one hand and cagA genotype ABCCC on the other hand with susceptibility to chronic gastritis and gastric cancer respectively.Conclusions: Overall, it can be concluded that the higher number of EPIYA-C copy numbers lead to the higher risk of gastric cancer. According to our results, it seems that the presence of EPIYA-ABCCC motif in strains of H. pylori should be considered as an appropriate marker in preventing the gastric cancer among the Iranian population.


Introduction: Helicobacter Pylori (H. Pylori) is a gram negative bacterium spiraled in the gastric epithelium. This bacterium is responsible for triggering benign inflammatory processes and is considered a carcinogenic agent. Methodology: This is a bibliographic review based on the analysis of published works, evaluating the relationship between H.Pylori and the development of gastric cancer based on keywords indexed in the DECs (described in science and health): “Helicobacter Pylori” “Cancer” “Stomach” “Gastric cancer” and information from INCA (National Cancer Institute). Result and Discussions: Helicobacter Pyloriinfection is associated with gastric neoplasms in which adenocarcinomas are the most prevalent, with more than 90% of cases. The diagnosis is made through EDA (Upper Digestive Endoscopy) with biopsy of the lesions and has a sensitivity of 97%. The treatment of H. pylori in the patient diagnosed with gastric cancer depends on the type of neoplasia. Conclusion: The relationship between H.Pylori and neoplastic processes is evident. Therefore, proper diagnosis and treatment in all carriers of the bacterium is essential in order to reduce the risk of developing gastric cancer.


2020 ◽  
Author(s):  
Marce-Amara Kpoghomou ◽  
jinchen Wang ◽  
Tianpei Wang ◽  
Guangfu Jin

Abstract Background: The association of Helicobacter pylori (H. pylori) babA2 gene with gastric cancer (GC) was reported by several studies, but results were inconsistent. This meta-analysis was performed to investigate the relationship between H. pylori babA2 gene and GC risk.Methods: Case-control studies involving the association between H. pylori babA2 gene and GC risk were systematically identified from PubMed databases. A meta-analysis was used to pool studies and to estimate odds ratios (ORs) with 95% confidence intervals (CIs) of H. pylori babA2 gene associated with GC risk.Results: Twenty studies were identified with a total of 1289 GC cases and 1081 controls. H. pylori babA2 gene was associated with an increased risk of GC by 2.05 fold (95% CI: 1.30-3.24, P=0.002). In subgroup analysis, we found that H. pylori babA2 gene was significantly associated with GC risk in Asian population (OR=2.63, 95% CI: 1.36-5.09 P=0.004) but not in South American population (OR=1.35, 95% CI: 0.69-2.64, P=0.379).Conclusions: This meta-analysis indicates that H. pylori babA2 gene may be associated with increased risk of GC, especially in Asian population.


Background and aim: Helicobacter pylori (H. pylori) is an incriminated pathogen causing diseases in both animals and humans and considered a zoonotic pathogen. H. pylori infection is considered a cause of gastric cancer, which rests a significant health care challenge. This study analyzes the expression pattern of matrix metalloprotein 2 (MMP-2) in patients with Helicobacter pylori-associated gastritis and the effect of H. pylori on gastric cancer stem cells, as well as study the role of helicon bacteriosis in dog in transmission of H. pylori infection to human. Materials and methods: Fifty-five of each sample (gastric biopsy, blood and stool) were collected from patients suffering from dyspepsia, chronic vomiting and perforated peptic ulcers and also from apparent healthy dogs. The investigation detected H. pylori by serological and histopathological examination. Biopsies were stored in physiological saline for identification of H. pylori by conventional time PCR. MMP-2 and Gastric cancer stem cells were then identified by immunohistochemistry. Results: Serological identification for H. pylori Antigen and Antibodies revealed (63% human, 50% dogs) and (87% human, 90% dogs) respectively were positive. Genotyping of H. pylori based on 16S rRNA gene showed 54.5% of human and 35% of dogs were positive. Immunohistochemistry revealed strong expression of CD44 in H. pylori- associated gastric cancer cases, MMP-2 expression was observed in all neoplastic lesions associated with H. pylori infection. Conclusion: H. pylori infection affects gastric mucosa and induces changes in gastric stem cells altering their differentiation and increased expression of MMP’s and CD44with a resultant potentiation of oncogenic alteration. In addition the up-regulation of both markers could be an instrumental to interpret the origination of gastric cancer.


2021 ◽  
Vol 22 (9) ◽  
pp. 4823
Author(s):  
María Fernanda González ◽  
Paula Díaz ◽  
Alejandra Sandoval-Bórquez ◽  
Daniela Herrera ◽  
Andrew F. G. Quest

Extracellular vesicles (EVs) are cell-derived vesicles important in intercellular communication that play an essential role in host-pathogen interactions, spreading pathogen-derived as well as host-derived molecules during infection. Pathogens can induce changes in the composition of EVs derived from the infected cells and use them to manipulate their microenvironment and, for instance, modulate innate and adaptive inflammatory immune responses, both in a stimulatory or suppressive manner. Gastric cancer is one of the leading causes of cancer-related deaths worldwide and infection with Helicobacter pylori (H. pylori) is considered the main risk factor for developing this disease, which is characterized by a strong inflammatory component. EVs released by host cells infected with H. pylori contribute significantly to inflammation, and in doing so promote the development of disease. Additionally, H. pylori liberates vesicles, called outer membrane vesicles (H. pylori-OMVs), which contribute to atrophia and cell transformation in the gastric epithelium. In this review, the participation of both EVs from cells infected with H. pylori and H. pylori-OMVs associated with the development of gastric cancer will be discussed. By deciphering which functions of these external vesicles during H. pylori infection benefit the host or the pathogen, novel treatment strategies may become available to prevent disease.


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