scholarly journals Interdisciplinary insights into the link between gut microbiome and gastric carcinogenesis—what is currently known?

2021 ◽  
Author(s):  
Karolina Kaźmierczak-Siedlecka ◽  
Agnieszka Daca ◽  
Giandomenico Roviello ◽  
Martina Catalano ◽  
Karol Połom
Keyword(s):  
Gastric Cancer ◽  
Gut Microbiome ◽  
Short Chain Fatty Acids ◽  
Gastric Carcinogenesis ◽  
Point Of View ◽  
Molecular Techniques ◽  
Nitroso Compounds ◽  
Gastric Microbiota ◽  
Development Of Gastric Cancer

AbstractCurrently, gastric cancer is one of the leading death-related cancer globally. The etiopathogenesis of gastric cancer is multifactorial and includes among others dysbiotic alterations of gastric microbiota. Molecular techniques revealed that stomach is not a sterile organ and it is resides with ecosystem of microbes. Due to the fact that the role of Helicobacter pylori infection in development of gastric cancer is established and well-studied, this paper is mainly focused on the role of other bacterial as well as viral and fungal gut microbiota imbalance in gastric carcinogenesis. Notably, not only the composition of gastric microbiota may play an important role in development of gastric cancer, but also its activity. Microbial metabolites, such as short-chain fatty acids, polyamines, N-nitroso compounds, and lactate, may significantly affect gastric carcinogenesis. Therefore, this paper discussed aforementioned aspects with the interdisciplinary insights (regarding also immunological point of view) into the association between gut microbiome and gastric carcinogenesis based on up-to-date studies.

The Role of Polymorphic Variants of Several Genes of Matrix Metalloproteinases and Their Tissue Inhibitors in the Development of Gastric Cancer

2021 ◽  
Vol 57 (5) ◽  
pp. 607-619
Author(s):  
L. F. Gallyamova ◽  
A. Kh. Nurgalieva ◽  
I. I. Khidiyatov ◽  
T. R. Nasibullin ◽  
F. R. Munasypov ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Matrix Metalloproteinases ◽  
Tissue Inhibitors ◽  
Polymorphic Variants ◽  
Development Of Gastric Cancer

scholarly journals SLCO4A1-AS1 Facilitates the Malignant Phenotype via miR-149-5p/STAT3 Axis in Gastric Cancer Cells

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Qing Li ◽  
Dachuan Zhang ◽  
Hui Wang ◽  
Jun Xie ◽  
Lei Peng ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Organic Anion ◽  
Organic Anion Transporter ◽  
Gastric Cancer Cells ◽  
Anion Transporter ◽  
Transporter Family ◽  
Cancer Tissues ◽  
Development Of Gastric Cancer

Solute carrier organic anion transporter family member 4A1 (SLCO4A1-AS1), a newly discovered lncRNA, may exert effects in tumors. Since its role in gastric cancer remains obscure, we sought to explore the mechanism of SLCO4A1-AS1 in gastric cancer. The relationship among SLCO4A1-AS1, miR-149-5p, and STAT3 was detected by bioinformatics, dual luciferase analysis, and Pearson’s test, and the expressions of these genes were determined by quantitative real-time PCR and Western blot. Moreover, CCK-8, flow cytometry, wound healing assay, and Transwell analysis were performed to verify the function of SLCO4A1-AS1 in gastric cancer. Rescue experiments were used to detect the role of miR-149-5p. The expressions of SLCO4A1-AS1 and STAT3 were increased, while the expression of miR-149-5p was suppressed in gastric cancer tissues and cell lines. In addition, STAT3 expression was negatively correlated with miR-149-5p expression but was positively correlated with SLCO4A1-AS1 expression. Overexpression of SLCO4A1-AS1 promoted cell viability, migration, invasion, and STAT3 expression but suppressed apoptosis, while knockdown of SLCO4A1-AS1 had the opposite effect. SLCO4A1-AS1 bound to miR-149-5p and targeted STAT3. Moreover, miR-149-5p mimic inhibited the malignant development of gastric cancer cells and obviously reversed the function of SLCO4A1-AS1 overexpression. Our research reveals that abnormally increased SLCO4A1-AS1 expression may be an important molecular mechanism in the development of gastric cancer.

scholarly journals Role of Bacterial Overgrowth in the Stomach as an Additional Risk Factor for Gastritis

2003 ◽  
Vol 17 (suppl b) ◽  
pp. 13B-17B ◽  
Author(s):  
Gregory Naylor ◽  
Anthony Axon
Keyword(s):  
Gastric Cancer ◽  
Cell Mass ◽  
Bacterial Overgrowth ◽  
Nitroso Compounds ◽  
Current Evidence ◽  
Additional Risk Factor ◽  
Proximal Small Bowel ◽  
Increased Risk ◽  
H Pylori

Gastric bacteria can either be ingested or ascend from the distal bowel; however, their survival is usually limited by gastric acidity and motility. A reduction in gastric acid can result in bacterial overgrowth in the stomach and proximal small bowel, and the number of organisms rises as the intragastric pH rises.The increased risk of noncardia gastric cancer seen in patients with hypochlorhydria may be explained by an excess of nitrites and N-nitroso compounds (NOCs). These compounds are found in the diet of populations with a high gastric cancer risk, but can also be produced by the organisms that exist in the hypochlorhydria stomach. It has long been hypothsized that nitrites and NOCs act as one of the triggers in the atrophy-metaplasia-dysplasia-carcinoma path. However, although indirect data have linked the premalignant changes of metaplasia and dysplasia to NOCs, direct measurement of gastric nitrites and NOCs has not confirmed such a link.The role ofHelicobacter pyloriin bacterial overgrowth is mainly as a cause of hypochlorhydria resulting from atrophic gastritis, leading to a reduction in the parietal cell mass.Acid-suppressing drugs can result in bacterial overgrowth and increased nitrites and NOCs, although there is no current evidence for an increased risk of gastric cancer in patients taking them. One explanation is that the stomach appears to be colonized by different organisms than those in patients with hypochlorhydria for other reasons. There is some evidence that bacterial overgrowth per se can cause gastric inflammation in mice; however, although in humans the degree of gastric inflammation is greater when overgrowth is more prominant this may simply reflect the greater degree of hypochlorhydria in patients with a more severe H pylori-induced inflammation.

scholarly journals Helicobacter pylori Infection and Gastric Dysbiosis: Can Probiotics Administration Be Useful to Treat This Condition?

2018 ◽  
Vol 2018 ◽  
pp. 1-7 ◽  
Author(s):  
Giovanni Bruno ◽  
Giulia Rocco ◽  
Piera Zaccari ◽  
Barbara Porowska ◽  
Maria Teresa Mascellino ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Lymphoid Tissue ◽  
Therapy Resistance ◽  
Mechanisms Of Action ◽  
Pathogenic Agent ◽  
The World ◽  
Gastric Microbiota ◽  
Common Infections

Helicobacter pylori (Hp) is responsible for one of the most common infections in the world. The prevalence exceeds 50% of the population in developing countries, and approximately one-third of the adults are colonized in North Europe and North America. It is considered a major pathogenic agent of chronic gastritis, peptic ulcer, atrophic gastritis, gastric cancer, and mucosa-associated lymphoid tissue lymphoma (MALT). Hp colonization modifies the composition of gastric microbiota that could drive the development of gastric disorders. Currently, an emerging problem in Hp treatment is represented by the increasing rate of antimicrobial therapy resistance. In this context, the search for adjuvant agents can be very useful to overcome this issue and probiotics administration can represent a valid option. The aim of this review is to describe the gastric microbiota changes during Hp colonization, the mechanisms of action, and a possible role of probiotics in the treatment of this infection.

scholarly journals The Crosstalk between Microbiome and Immune Response in Gastric Cancer

2020 ◽  
Vol 21 (18) ◽  
pp. 6586
Author(s):  
Rihab Nasr ◽  
Ali Shamseddine ◽  
Deborah Mukherji ◽  
Farah Nassar ◽  
Sally Temraz
Keyword(s):  
Gastric Cancer ◽  
Immune Response ◽  
Gut Microbiome ◽  
Tumor Antigens ◽  
Checkpoint Inhibitors ◽  
Specific Antigen ◽  
Cell Responses ◽  
Host Epithelium ◽  
H Pylori

Gastric cancer is the end result of a complex interplay between host genetics, environmental factors, and microbial factors. The link between gut microbiome and gastric cancer has been attributed to persistent activation of the host’s immune system by gut microbiota. The end result of this dysregulated interaction between host epithelium and microbes is a state of chronic inflammation. Gut bacteria can promote anti-tumor immune responses through several mechanisms. These include triggering T-cell responses to bacterial antigens that can cross-react with tumor antigens or cause tumor-specific antigen recognition; engagement of pattern recognition receptors that mediate pro-immune or anti-inflammatory effects or via small metabolites that mediate systemic effects on the host. Here we review the role of the gut microbiome including H. pylori and non-H. pylori gastric bacteria, the immune response, and immunotherapy using checkpoint inhibitors. We also review the evidence for cross talk between the gut microbiome and immune response in gastric cancer.

scholarly journals The Role of PPARγinHelicobacter pyloriInfection and Gastric Carcinogenesis

PPAR Research ◽  
2012 ◽  
Vol 2012 ◽  
pp. 1-6 ◽  
Author(s):  
Jong-Min Lee ◽  
Sung Soo Kim ◽  
Young-Seok Cho
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Current Knowledge ◽  
Mucosal Injury ◽  
Gastric Carcinogenesis ◽  
Etiologic Factor ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
H Pylori

Peroxisome proliferator-activated receptorγ(PPARγ) is a nuclear receptor that is important in many physiological and pathological processes, such as lipid metabolism, insulin sensitivity, inflammation, cell proliferation, and carcinogenesis. Several studies have shown that PPARγplays an important role in gastric mucosal injury due toHelicobacter pylori(H. pylori). AsH. pyloriinfection is the main etiologic factor in chronic gastritis and gastric cancer, understanding of the potential roles of PPARγinH. pyloriinfection may lead to the development of a therapeutic target. In this paper, the authors discuss the current knowledge on the role of PPARγinH. pyloriinfection and its related gastric carcinogenesis.

scholarly journals The uninvited guests of our microbiome: Helicobacter pylori and Epstein-Barr virus and their role in gastric cancerogenesis

2021 ◽  
Vol 75 (1) ◽  
pp. 611-619
Author(s):  
Magdalena Dzikowiec ◽  
Dorota Pastuszak-Lewandoska
Keyword(s):  
Gastric Cancer ◽  
Epstein Barr Virus ◽  
Human Microbiome ◽  
Infectious Agents ◽  
Gastrointestinal Microbiome ◽  
Barr Virus ◽  
Epstein Barr ◽  
H Pylori ◽  
Development Of Gastric Cancer

Abstract It is well established that human body is an ecosystem for numerous microorganisms: bacteria, fungi, eukaryotic parasites, and viruses. They form a “microbiome” that under conditions of homeostasis remains in a friendly mutual relationship with the host. However, the composition and diversity of this microbe community is dynamic and can be changed under the influence of environmental factors, such as diet, antibiotic therapy, lifestyle, and the host’s genotype and immunity. The result of gut microbiome dysbiosis can lead even to cancer. The aim of this review is the description of the healthy gastrointestinal microbiome and the role of two infectious agents: Gram-negative bacteria Helicobacter pylori and Epstein-Barr virus in the development of gastric cancer in terms of gut dysbiosis. H. pylori is the most important pathogen of gastric microbiome with clear impact on its diversity. Coinfection with Epstein-Barr virus causes chronic gastritis, and the inflammatory process is significantly increased. The process of carcinogenesis begins with chronic inflammation that causes atrophic gastritis, intestinal metaplasia, dysplasia, and finally cancer. It has been proven that chronic inflammatory infection caused by infectious agents increases the risk of stomach cancer. Molecular methods that are progressively used to explore the human microbiome provide hope that this knowledge will be used for future diagnoses and therapy in the state of its dysbiosis and in cases of gastric cancer.

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