scholarly journals Dysregulation of lncRNA in Helicobacter pylori-Infected Gastric Cancer Cells

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Leila Yousefi ◽  
Hamid Owaysee Osquee ◽  
Reza Ghotaslou ◽  
Mohammad Ahangarzadeh Rezaee ◽  
Tahereh Pirzadeh ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Noncoding Rnas ◽  
Bacterial Virulence ◽  
Cancer Development ◽  
Biological Macromolecules ◽  
Gastric Cancer Cells ◽  
Protein Coding ◽  
Protein Coding Genes ◽  
H Pylori

Helicobacter pylori (H. pylori) infection is the most common cause of gastric cancer (GC). This microorganism is genetically diverse; GC is caused by several genetic deregulations in addition to environmental factors and bacterial virulence factors. lncRNAs (long noncoding RNAs) are significant biological macromolecules in GC, have specific functions in diseases, and could be therapeutic targets. Altered lncRNAs can lead to the abnormal expression of adjacent protein-coding genes, which may be important in cancer development. Their mechanisms have not been well understood, so we are going to investigate the risk of GC in a population with both high lncRNA and H. pylori infection.

scholarly journals Role of TNF-α-Inducing Protein Secreted by Helicobacter pylori as a Tumor Promoter in Gastric Cancer and Emerging Preventive Strategies

Toxins ◽  
2021 ◽  
Vol 13 (3) ◽  
pp. 181
Author(s):  
Masami Suganuma ◽  
Tatsuro Watanabe ◽  
Eisaburo Sueoka ◽  
In Kyoung Lim ◽  
Hirota Fujiki
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Cell Surface Receptor ◽  
Tumor Promoter ◽  
Cancer Development ◽  
Human Gastric Cancer ◽  
Tnf Α ◽  
Surface Receptor ◽  
H Pylori ◽  
Factor Α

The tumor necrosis factor-α (TNF-α)-inducing protein (tipα) gene family, comprising Helicobacter pylori membrane protein 1 (hp-mp1) and tipα, has been identified as a tumor promoter, contributing to H. pylori carcinogenicity. Tipα is a unique H. pylori protein with no similarity to other pathogenicity factors, CagA, VacA, and urease. American H. pylori strains cause human gastric cancer, whereas African strains cause gastritis. The presence of Tipα in American and Euro-Asian strains suggests its involvement in human gastric cancer development. Tipα secreted from H. pylori stimulates gastric cancer development by inducing TNF-α, an endogenous tumor promoter, through its interaction with nucleolin, a Tipα receptor. This review covers the following topics: tumor-promoting activity of the Tipα family members HP-MP1 and Tipα, the mechanism underlying this activity of Tipα via binding to the cell-surface receptor, nucleolin, the crystal structure of rdel-Tipα and N-terminal truncated rTipα, inhibition of Tipα-associated gastric carcinogenesis by tumor suppressor B-cell translocation gene 2 (BTG2/TIS21), and new strategies to prevent and treat gastric cancer. Thus, Tipα contributes to the carcinogenicity of H. pylori by a mechanism that differs from those of CagA and VacA.

scholarly journals Inhibitory Effect of β-Carotene on Helicobacter pylori-Induced TRAF Expression and Hyper-Proliferation in Gastric Epithelial Cells

Antioxidants ◽  
2019 ◽  
Vol 8 (12) ◽  
pp. 637 ◽  
Author(s):  
Yongchae Park ◽  
Hanbit Lee ◽  
Joo Weon Lim ◽  
Hyeyoung Kim
Keyword(s):  
Gene Expression ◽  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Epithelial Cells ◽  
Nadph Oxidase ◽  
Gastric Epithelial Cells ◽  
Gastric Cancer Cells ◽  
Ags Cells ◽  
H Pylori ◽  
Β Carotene

Helicobacter pylori infection causes the hyper-proliferation of gastric epithelial cells that leads to the development of gastric cancer. Overexpression of tumor necrosis factor receptor associated factor (TRAF) is shown in gastric cancer cells. The dietary antioxidant β-carotene has been shown to counter hyper-proliferation in H. pylori-infected gastric epithelial cells. The present study was carried out to examine the β-carotene mechanism of action. We first showed that H. pylori infection decreases cellular IκBα levels while increasing cell viability, NADPH oxidase activity, reactive oxygen species production, nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) activation, and TRAF1 and TRAF2 gene expression, as well as protein–protein interaction in gastric epithelial AGS cells. We then demonstrated that pretreatment of cells with β-carotene significantly attenuates these effects. Our findings support the proposal that β-carotene has anti-cancer activity by reducing NADPH oxidase-mediated production of ROS, NF-κB activation and NF-κB-regulated TRAF1 and TRAF2 gene expression, and hyper-proliferation in AGS cells. We suggest that the consumption of β-carotene-enriched foods could decrease the incidence of H. pylori-associated gastric disorders.

The regulatory role of exosomal CagA and microRNAs derived from H. pylori-related gastric cancer cells on signaling pathways related to cancer development: a bioinformatics aspect

2020 ◽  
Vol 29 (6) ◽  
pp. 1295-1312
Author(s):  
Nazila Bostanshirin ◽  
Ahmad Bereimipour ◽  
Mohammad ali Pahlevan Neshan ◽  
Mina Aghasafi ◽  
Romina Mehtararaghinia ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Signaling Pathways ◽  
Cancer Development ◽  
Regulatory Role ◽  
Gastric Cancer Cells ◽  
H Pylori

scholarly journals Nanomechanical Hallmarks of Helicobacter pylori Infection in Pediatric Patients

2021 ◽  
Vol 22 (11) ◽  
pp. 5624
Author(s):  
Piotr Deptuła ◽  
Łukasz Suprewicz ◽  
Tamara Daniluk ◽  
Andrzej Namiot ◽  
Sylwia Joanna Chmielewska ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Mechanical Properties ◽  
Helicobacter Pylori ◽  
Mechanical Response ◽  
Cellular Level ◽  
Cancer Development ◽  
Tissue Samples ◽  
Diagnostic Measures ◽  
Gastric Cells ◽  
H Pylori

Background: the molecular mechanism of gastric cancer development related to Helicobacter pylori (H. pylori) infection has not been fully understood, and further studies are still needed. Information regarding nanomechanical aspects of pathophysiological events that occur during H. pylori infection can be crucial in the development of new prevention, treatment, and diagnostic measures against clinical consequences associated with H. pylori infection, including gastric ulcer, duodenal ulcer, and gastric cancer. Methods: in this study, we assessed mechanical properties of children’s healthy and H. pylori positive stomach tissues and the mechanical response of human gastric cells exposed to heat-treated H. pylori cells using atomic force microscopy (AFM NanoWizard 4 BioScience JPK Instruments Bruker). Elastic modulus (i.e., the Young’s modulus) was derived from the Hertz–Sneddon model applied to force-indentation curves. Human tissue samples were evaluated using rapid urease tests to identify H. pylori positive samples, and the presence of H. pylori cells in those samples was confirmed using immunohistopathological staining. Results and conclusion: collected data suggest that nanomechanical properties of infected tissue might be considered as markers indicated H. pylori presence since infected tissues are softer than uninfected ones. At the cellular level, this mechanical response is at least partially mediated by cell cytoskeleton remodeling indicating that gastric cells are able to tune their mechanical properties when subjected to the presence of H. pylori products. Persistent fluctuations of tissue mechanical properties in response to H. pylori infection might, in the long-term, promote induction of cancer development.

scholarly journals Engagement of CEACAM1 by Helicobacter pylori HopQ Is Important for the Activation of Non-Canonical NF-κB in Gastric Epithelial Cells

2021 ◽  
Vol 9 (8) ◽  
pp. 1748
Author(s):  
Karin Taxauer ◽  
Youssef Hamway ◽  
Anna Ralser ◽  
Alisa Dietl ◽  
Karin Mink ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Epithelial Cells ◽  
Surface Protein ◽  
Host Cells ◽  
Gastric Epithelial Cells ◽  
Gastric Cancer Cells ◽  
Tissue Samples ◽  
Mutant Strains ◽  
H Pylori

The gastric pathogen Helicobacter pylori infects half of the world’s population and is a major risk factor for gastric cancer development. In order to attach to human gastric epithelial cells and inject the oncoprotein CagA into host cells, H. pylori utilizes the outer membrane protein HopQ that binds to the cell surface protein CEACAM, which can be expressed on the gastric mucosa. Once bound, H. pylori activates a number of signaling pathways, including canonical and non-canonical NF-κB. We investigated whether HopQ–CEACAM interaction is involved in activating the non-canonical NF-κB signaling pathway. Different gastric cancer cells were infected with the H. pylori wild type, or HopQ mutant strains, and the activation of non-canonical NF-κB was related to CEACAM expression levels. The correlation between CEACAM levels and the activation of non-canonical NF-κB was confirmed in human gastric tissue samples. Taken together, our findings show that the HopQ–CEACAM interaction is important for activation of the non-canonical NF-κB pathway in gastric epithelial cells.

scholarly journals Gastric Cancer and Associated Pathogens: Is There Any Association in Moroccan Region?

2021 ◽  
Author(s):  
Samia Alaoui Boukhris ◽  
Mounia El khadir ◽  
Safae Karim ◽  
Tiatou Souho ◽  
Dafr-Allah Benajah ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Retrospective Study ◽  
Epstein Barr Virus ◽  
University Hospital ◽  
Cancer Development ◽  
Barr Virus ◽  
Epstein Barr ◽  
H Pylori

Abstract Purpose: Helicobacter pylori, Epstein-Barr virus and human papillomavirus are three pathogens associated with various human cancers. This study aimed to investigate the role of these pathogens in gastric cancer in Moroccan population Methods: For this, a retrospective study has been conducted on participants attending the gastroenterology department of Hassan II University Hospital of Fez. A total of 279 participants were enrolled. H. pylori, EBV and HPV were detected and genotyped by PCR.Results: A significant association has been established between H. pylori, EBV and gastric cancer. 93.4% and 43.3% of gastric cancer cases are related to H. pylori and EBV respectively (p≤0.01). H. pylori-EBV co-infection is responsible of 31.6% of gastric cancer cases (p<0.01). Correlation between pathogens genotypes and gastric cancer shows 55.6% of GC EBV positives are carrying the 30bp deletion in LMP1gene, while 16% of gastric cancers cases are carrying high-risk genotypes of HPV (p=0.21). Conclusion: The obtained results highlight the possible role of co-infection in gastric cancer development.

scholarly journals Eradication Treatment of Helicobacter pylori Infection: Its Importance and Possible Relationship in Preventing the Development of Gastric Cancer

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Bruna Maria Roesler ◽  
Sandra Cecília Botelho Costa ◽  
José Murilo Robilotta Zeitune
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Genetic Factors ◽  
Salt Intake ◽  
Mucosal Damage ◽  
Bacterial Virulence ◽  
Host Genetic ◽  
H Pylori ◽  
Host Genetic Factors ◽  
Development Of Gastric Cancer

Helicobacter pylori is the most important carcinogen for gastric adenocarcinoma. Bacterial virulence factors are essential players in modulating the immune response involved in the initiation of carcinogenesis in the stomach; host genetic factors contribute to the regulation of the inflammatory response and to the aggravation of mucosal damage. In terms of environmental factors, salt intake and smoking contribute to the development of lesions. Various therapeutic schemes are proposed to eradicate H. pylori infection, which could potentially prevent gastric cancer, offering the greatest benefit if performed before premalignant changes of the gastric mucosa have occurred.

scholarly journals Inhibition of Helicobacter pylori and Gastric Cancer Cells by Lipid Aldehydes from Viburnum opulus (Adoxaceae)

2007 ◽  
Vol 2 (10) ◽  
pp. 1934578X0700201
Author(s):  
Maria Teresa Laux ◽  
Manuel Aregullin ◽  
Eloy Rodriguez
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Gastric Cancer Cell Line ◽  
Cancer Cell Line ◽  
Peptic Ulcers ◽  
Viburnum Opulus ◽  
Gastric Cancer Cells ◽  
H Pylori ◽  
Lipid Aldehydes

A unique group of bioactive, naturally occurring lipid aldehydes were isolated from the fruits of Viburnum opulus, (family Adoxaceae). The natural occurrences of these fatty acid derived aldehydes are reported here for the first time. Helicobacter pylori is a prevalent gastroduodenal pathogen, a causal agent of chronic gastritis and peptic ulcers and an important co-factor in gastric cancer development. We investigated the chemistry and bioactivity of these active constituents by evaluating their ability to inhibit the growth of H. pylori and to induce apoptosis in a gastric cancer cell line (CRL-5971) in vitro.

scholarly journals Helicobacter pylori Infection-Induced Hepatoma-Derived Growth Factor Regulates the Differentiation of Human Mesenchymal Stem Cells to Myofibroblast-Like Cells

Cancers ◽  
2018 ◽  
Vol 10 (12) ◽  
pp. 479 ◽  
Author(s):  
Chung-Jung Liu ◽  
Yao-Kuang Wang ◽  
Fu-Chen Kuo ◽  
Wen-Hung Hsu ◽  
Fang-Jung Yu ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Stem Cells ◽  
Helicobacter Pylori ◽  
Mesenchymal Stem Cells ◽  
Growth Factor ◽  
Tumor Cell ◽  
Critical Role ◽  
Human Gastric Cancer ◽  
Gastric Cancer Cells ◽  
H Pylori

Hepatoma-derived growth factor (HDGF) plays a critical role in tumor cell proliferation, anti-apoptosis, VEGF expression, lymph node metastasis and poor prognosis in human gastric cancer. Gastric cancer, as one of the most prevalent cancers worldwide, is the second leading cause of cancer-related mortality in the world for the prognosis of gastric cancer is generally poor, especially in patients with advanced stage. Helicobacter pylori (H. pylori) infection causes the chronic inflammation of stomach as well as the development of gastric cancer, with a three to six-fold increased risk of gastric cancer. Carcinoma-associated fibroblasts (CAFs) are myofibroblasts in tumor microenvironment, which possess various abilities to promote the progression of cancer by stimulating neoangiogenesis, proliferation, migration, invasion and therapy resistance of tumor cell. Mesenchymal stem cells (MSCs) are reported to promote tumor malignance through differentiation of MSCs toward CAFs. In the present study, we demonstrated that H. pylori infection promotes HDGF expression in human gastric cancer cells. HBMMSCs treated with HDGF assume properties of CAF-like myofibroblastic phenotypes, including expression of myofibroblast markers (α-smooth muscle actin (α-SMA), procollagen α1, tropomyoson I, desmin, fibroblast activation protein (FAP)), and fibroblast markers (prolyl-4-hydroxylase A1 (PHA1) and fibroblast specific protein-1 (FSP-1)/S100A4). HDGF recruits HBMMSCs, and then HBMMSCs further contributes to cell survival and invasive motility in human gastric cancer cells. Treatment of HDGF neutralizing antibody (HDGF-NAb) and serum significantly inhibit HDGF-regulated differentiation and recruitment of HBMMSCs. These findings suggest that HDGF might play a critical role in gastric cancer progress through stimulation of HBMMSCs differentiation to myofibroblast-like cells.

scholarly journals Helicobacter pylori-Mediated Immunity and Signaling Transduction in Gastric Cancer

2020 ◽  
Vol 9 (11) ◽  
pp. 3699
Author(s):  
Nozomi Ito ◽  
Hironori Tsujimoto ◽  
Hideki Ueno ◽  
Qian Xie ◽  
Nariyoshi Shinomiya
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Cancer Cells ◽  
Signaling Pathways ◽  
Cancer Progression ◽  
Intracellular Signaling ◽  
Cellular Proliferation ◽  
Gastric Cancer Cells ◽  
Downstream Signaling ◽  
H Pylori

Helicobacter pylori infection is a leading cause of gastric cancer, which is the second-most common cancer-related death in the world. The chronic inflammatory environment in the gastric mucosal epithelia during H. pylori infection stimulates intracellular signaling pathways, namely inflammatory signals, which may lead to the promotion and progression of cancer cells. We herein report two important signal transduction pathways, the LPS-TLR4 and CagA-MET pathways. Upon H. pylori stimulation, lipopolysaccharide (LPS) binds to toll-like receptor 4 (TLR4) mainly on macrophages and gastric epithelial cells. This induces an inflammatory response in the gastric epithelia to upregulate transcription factors, such as NF-κB, AP-1, and IRFs, all of which contribute to the initiation and progression of gastric cancer cells. Compared with other bacterial LPSs, H. pylori LPS has a unique function of inhibiting the mononuclear cell (MNC)-based production of IL-12 and IFN-γ. While this mechanism reduces the degree of inflammatory reaction of immune cells, it also promotes the survival of gastric cancer cells. The HGF/SF-MET signaling plays a major role in promoting cellular proliferation, motility, migration, survival, and angiogenesis, all of which are essential factors for cancer progression. H. pylori infection may facilitate MET downstream signaling in gastric cancer cells through its CagA protein via phosphorylation-dependent and/or phosphorylation-independent pathways. Other signaling pathways involved in H. pylori infection include EGFR, FAK, and Wnt/β-Catenin. These pathways function in the inflammatory process of gastric epithelial mucosa, as well as the progression of gastric cancer cells. Thus, H. pylori infection-mediated chronic inflammation plays an important role in the development and progression of gastric cancer.

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