Abstract
Helicobacter pylori (H. pylori) is one of the most common human pathogens, affecting half of the world’s population. Approximately 20% of the infected patients develop gastric ulcers or neoplastic changes in the gastric stroma. An infection also leads to the progression of epithelial–mesenchymal transition within gastric tissue, increasing the probability of gastric cancer development. This paper aims to review the role of H. pylori and its virulence factors in epithelial–mesenchymal transition associated with malignant transformation within the gastric stroma. The reviewed factors included: CagA (cytotoxin-associated gene A) along with induction of cancer stem-cell properties and interaction with YAP (Yes-associated protein pathway), tumor necrosis factor α-inducing protein, Lpp20 lipoprotein, Afadin protein, penicillin-binding protein 1A, microRNA-29a-3p, programmed cell death protein 4, lysosomal-associated protein transmembrane 4β, cancer-associated fibroblasts, heparin-binding epidermal growth factor (HB-EGF), matrix metalloproteinase-7 (MMP-7), and cancer stem cells (CSCs). The review summarizes the most recent findings, providing insight into potential molecular targets and new treatment strategies for gastric cancer.
Highlights
Helicobacter pylori (H. pylori) is a helix-shaped, Gram-negative, microaerophilic, flagellated bacterium that is capable of biofilm formation and converting from spiral to coccoid form [1,2,3,4,5,6].It is a highly invasive microorganism responsible for one of the highest prevalences of chronic infections worldwide, even though over 80% of infected patients remain asymptomatic [7,8,9,10,11,12,13]
This review summarizes several mechanisms associated with epithelial–mesenchymal transition, gastric tumor microenvironment, and the influence of H. pylori infection, some described mechanisms are H. pylori-specific
The relevance of the infection by cytotoxin-associated gene A (CagA)-positive H. pylori strain on Epithelial–mesenchymal transition (EMT) in gastric cancer was confirmed by significantly higher expression of CD44 and mesenchymal markers in tumor samples
Summary
Helicobacter pylori (H. pylori) is a helix-shaped, Gram-negative, microaerophilic, flagellated bacterium that is capable of biofilm formation and converting from spiral to coccoid form [1,2,3,4,5,6]. H. pylori infection significantly affects the gastric microenvironment by induction of several inflammatory responses via infiltrating macrophages, neutrophils, regulatory T-cells, and natural killer cells [84,85]. Inflammatory mediators such as cytokines, chemokines, and metalloproteinases. A significant number of H. pylori virulence factors are considered being associated with the promotion of EMT in gastric cells, which causes neoplasia and malignant transformation. Even though H. pylori-induced carcinogenesis is not fully understood, several mechanisms have already been deciphered
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