Helicobacter pylori induces malignant transformation of gastric epithelial cells in vitro

Yu, Xiuwen; Xu, Ying; Gong, Yuehua; Xu, Qian; Yuan, Yuan

doi:10.1111/j.1600-0463.2010.02709.x

Cited by 17 publications

(10 citation statements)

References 29 publications

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“…Although only H.pylori is associated with the activation of E-cadherin/β-catenin/TCF-4 signaling pathway in normal gastric epithelial cells (Yu et al, 2011 , 2014 ), both pathogens are linked to the activation of NF-κβ and MAP kinases oncogenic pathways in GC cell lines (Mohr et al, 2014 ; Liu and Cohen, 2015 ; Byun et al, 2016 ; Dela Pena-Ponce et al, 2017 ). Co-infection by EBV can also hinder the host response to H. pylori .…”

Section: Infectious Agents In Gastric Cancermentioning

confidence: 99%

Role of microRNAs and Exosomes in Helicobacter pylori and Epstein-Barr Virus Associated Gastric Cancers

et al. 2018

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Emerging evidence suggests that chronic inflammation caused by pathogen infection is connected to the development of various types of cancer. It is estimated that up to 20% of all cancer deaths is linked to infections and inflammation. In gastric cancer, such triggers can be infection of the gastric epithelium by either Helicobacter pylori (H. pylori), a bacterium present in half of the world population; or by Epstein-Barr virus (EBV), a double-stranded DNA virus which has recently been associated with gastric cancer. Both agents can establish lifelong inflammation by evolving to escape immune surveillance and, under certain conditions, contribute to the development of gastric cancer. Non-coding RNAs, mainly microRNAs (miRNAs), influence the host innate and adaptive immune responses, though long non-coding RNAs and viral miRNAs also alter these processes. Reports suggest that chronic infection results in altered expression of host miRNAs. In turn, dysregulated miRNAs modulate the host inflammatory immune response, favoring bacterial survival and persistence within the gastric mucosa. Given the established roles of miRNAs in tumorigenesis and innate immunity, they may serve as an important link between H. pylori- and EBV-associated inflammation and carcinogenesis. Example of this is up-regulation of miR-155 in H. pylori and EBV infection. The tumor environment contains a variety of cells that need to communicate with each other. Extracellular vesicles, especially exosomes, allow these cells to deliver certain type of information to other cells promoting cancer growth and metastasis. Exosomes have been shown to deliver not only various types of genetic information, mainly miRNAs, but also cytotoxin-associated gene A (CagA), a major H. pylori virulence factor. In addition, a growing body of evidence demonstrates that exosomes contain genetic material of viruses and viral miRNAs and proteins such as EBV latent membrane protein 1 (LMP1) which are delivered into recipient cells. In this review, we focus on the dysregulated H. pylori- and EBV-associated miRNAs while trying to unveil possible causal mechanisms. Moreover, we discuss the role of exosomes as vehicles for miRNA delivery in H. pylori- and EBV-related carcinogenesis.

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Section: Infectious Agents In Gastric Cancermentioning

confidence: 99%

Role of microRNAs and Exosomes in Helicobacter pylori and Epstein-Barr Virus Associated Gastric Cancers

et al. 2018

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“…Another study also suggests that EBV and H. pylori transform the stomach epithelium cells and play roles in carcinogenesis [78]. Both pathogens induce common pathways which leads to the activation of transforming factors in stomach epithelial cells by β -catenin/TCF-4 signalling pathway [79, 285]. In another study, an association between EBV and H. pylori copositivity was shown and significant infiltration in premalignant lesions in GC was observed [78].…”

Section: Ebv and H Pylori Factors Contributing To The Developmentmentioning

confidence: 99%

Status of Epstein-Barr Virus Coinfection withHelicobacter pyloriin Gastric Cancer

Singh

Jha

2017

Journal of Oncology

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Epstein-Barr virus is a ubiquitous human herpesvirus whose primary infection causes mononucleosis, Burkett's lymphoma, nasopharyngeal carcinoma, autoimmune diseases, and gastric cancer (GC). The persistent infection causes malignancies in lymph and epithelial cells. Helicobacter pylori causes gastritis in human with chronic inflammation. This chronic inflammation is thought to be the cause of genomic instability. About 45%-word population have a probability of having both pathogens, namely, H. pylori and EBV. Approximately 180 per hundred thousand population is developing GC along with many gastric abnormalities. This makes GC the third leading cause of cancer-related death worldwide. Although lots of research are carried out individually for EBV and H. pylori, still there are very few reports available on coinfection of both pathogens. Recent studies suggested that EBV and H. pylori coinfection increases the occurrence of GC as well as the early age of GC detection comparing to individual infection. The aim of this review is to present status on coinfection of both pathogens and their association with GC.

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“…H. pylori infection is known to be associated with the development of gastritis, peptic ulcers, chronic atrophy, and gastric adenocarcinoma (Suerbaum and Michetti, 2002;Yu et al, 2011;Makobongo et al, 2014;Seo et al, 2014). However, the molecular mechanisms by which H. pylori contributes to the development of gastric diseases remain to be elucidated.…”

Section: Introductionmentioning

confidence: 98%

Morphological changes in human gastric epithelial cells induced by nuclear targeting of Helicobacter pylori urease subunit A

et al. 2015

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Nuclear targeting of bacterial proteins and their pathological effects on host cells are an emerging pathogenic mechanism in bacteria. We have previously reported that urease subunit A (UreA) of Helicobacter pylori targets the nuclei of COS-7 cells through nuclear localization signals (NLSs). This study further investigated whether UreA of H. pylori targets the nuclei of gastric epithelial cells and then induces molecular and cellular changes in the host cells. H. pylori 26695 strain produced and secreted outer membrane vesicles (OMVs). UreA was translocated into gastric epithelial AGS cells through outer membrane vesicles (OMVs) and then targeted the nuclei of AGS cells. Nuclear targeting of rUreA did not induce host cell death, but resulted in morphological changes, such as cellular elongation, in AGS cells. In contrast, AGS cells treated with rUreA?NLS proteins did not show this morphological change. Next generation sequencing revealed that nuclear targeting of UreA differentially regulated 102 morphogenesis- related genes, of which 67 and 35 were up-regulated and down-regulated, respectively. Our results suggest that nuclear targeting of H. pylori UreA induces both molecular and cellular changes in gastric epithelial cells.

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Helicobacter pylori induces malignant transformation of gastric epithelial cells in vitro

Cited by 17 publications

References 29 publications

Role of microRNAs and Exosomes in Helicobacter pylori and Epstein-Barr Virus Associated Gastric Cancers

Role of microRNAs and Exosomes in Helicobacter pylori and Epstein-Barr Virus Associated Gastric Cancers

Status of Epstein-Barr Virus Coinfection withHelicobacter pyloriin Gastric Cancer

Morphological changes in human gastric epithelial cells induced by nuclear targeting of Helicobacter pylori urease subunit A

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