Molecular Mechanism of Helicobacter pylori-Induced Gastric Cancer

Alipour, Majid

doi:10.1007/s12029-020-00518-5

Cited by 154 publications

(109 citation statements)

References 102 publications

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“…The list of such diseases is wide and continues to grow, including: chronic otitis media/sinuses, endocarditis, lung infections associated with cystic fibrosis, urinary tract infections, vaginosis, osteomyelitis, chronic wound infections, catheter-related infections, and cancers of bile ducts and digestive system [ 4 , 5 , 8 ]. In the context of the last type of infections, attention should be focused strongly on spiral, Gram-negative rods colonizing the gastric mucosa— Helicobacter pylori [ 9 , 10 ].…”

Section: The Issue Of Biofilm Formation In the Biomedical Sectormentioning

confidence: 99%

Biofilm Formation as a Complex Result of Virulence and Adaptive Responses of Helicobacter pylori

et al. 2020

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Helicobacter pylori is a bacterium that is capable of colonizing a host for many years, often for a lifetime. The survival in the gastric environment is enabled by the production of numerous virulence factors conditioning adhesion to the mucosa surface, acquisition of nutrients, and neutralization of the immune system activity. It is increasingly recognized, however, that the adaptive mechanisms of H. pylori in the stomach may also be linked to the ability of this pathogen to form biofilms. Initially, biofilms produced by H. pylori were strongly associated by scientists with water distribution systems and considered as a survival mechanism outside the host and a source of fecal-oral infections. In the course of the last 20 years, however, this trend has changed and now the most attention is focused on the biomedical aspect of this structure and its potential contribution to the therapeutic difficulties of H. pylori. Taking into account this fact, the aim of the current review is to discuss the phenomenon of H. pylori biofilm formation and present this mechanism as a resultant of the virulence and adaptive responses of H. pylori, including morphological transformation, membrane vesicles secretion, matrix production, efflux pump activity, and intermicrobial communication. These mechanisms will be considered in the context of transcriptomic and proteomic changes in H. pylori biofilms and their modulating effect on the development of this complex structure.

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Section: The Issue Of Biofilm Formation In the Biomedical Sectormentioning

confidence: 99%

Biofilm Formation as a Complex Result of Virulence and Adaptive Responses of Helicobacter pylori

et al. 2020

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“…Upon entering the cytoplasm of gastric epithelial cells via a “molecular syringe” typical of bacterial type IV secretion systems (T4SS), CagA undergoes tyrosine phosphorylation triggering it to act as a mitogen by activating the Ras/Raf/MAPK/ERK pathway [ 27 , 28 ] (a well-known major pro-oncogenic pathway which signals for cellular proliferation). Activation of the MAPK/ERK pathway further induces the “hummingbird” phenotype, which is characterised by an elongated shape reminiscent of epithelial mesenchymal transition (EMT) and increased cell motility [ 29 ].…”

Section: Implications Of H Pylorimentioning

confidence: 99%

“… Activation of several inflammatory pathways known to produce cytokines mediated by H. pylori infection. CagA injected via T4SS which is phosphorylated by Src activates Ras/Raf/MAPK/ERK via SHP-2 [ 27 ]; nuclear translocation of ERK subsequently induces ETS like-1 protein (ELK1) and serum response factor (SRF) binding to the serum response element (SRE) leading to transcription of AP-1 [ 28 ]. STAT3 dimerisation and nuclear translocation also occurs after CagA mediated activation of JAK.…”

Section: Figurementioning

confidence: 99%

Peripheral Cytokine Levels as a Prognostic Indicator in Gastric Cancer: A Review of Existing Literature

Yang

Chua

et al. 2021

Biomedicines

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Although strong connections exist between the carcinogenesis of gastric cancer and chronic inflammation, gastric cancer is unique in that the chronic gastritis which frequently precedes carcinogenesis is strongly associated with H. pylori infection. The interplay between H. pylori virulence factors and host immune cells is complex but culminates in the activation of inflammatory pathways and transcription factors such as NF-κB, STAT3, and AP-1, all of which upregulate cytokine production. Due to the key role of cytokines in modulating the immune response against tumour cells as well as possibly stimulating tumour growth and proliferation, different patterns of cytokine secretion may be associated with varying patient outcomes. In relation to gastric cancer, interleukin-6, 8, 10, 17A, TNF, and IFN-γ may have pro-tumour properties, although interleukin-10, TNF, and IFN-γ may have anti-tumour effects. However, due to the lack of studies investigating patient outcomes, only a link between higher interleukin-6 levels and poorer prognosis has been demonstrated. Further investigations which link peripheral cytokine levels to patient prognosis may elucidate important pathological mechanisms in gastric cancer which adversely impact patient survival and allow treatments targeting these processes to be developed.

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“…Despite the inflammatory response, Helicobacter pylori is capable of evading the antibacterial immune reaction [ 26 , 27 , 28 , 29 , 30 , 31 ]. Although the significance of cagA gene and proteins for the bacterial physiology has yet to be fully elucidated [ 26 , 30 , 31 , 32 ], the cagA protein has been shown to be a marker of the cag pathogenicity island of Helicobacter pylori, and several studies have revealed that intestinal metaplasia, sporadic gastric cancer and mucosa-associated lymphoid tissue (MALT) lymphoma are most commonly found in subjects infected with cagA -positive strains [ 28 , 33 , 34 , 35 , 36 ].…”

Section: Gastric Cancer: Sporadic and Hereditary Formsmentioning

confidence: 99%

Advances in the Aetiology & Endoscopic Detection and Management of Early Gastric Cancer

Kohoutová

Banks

Bureš

2021

Cancers

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The mortality rates of gastric carcinoma remain high, despite the progress in research and development in disease mechanisms and treatment. Therefore, recognition of gastric precancerous lesions and early neoplasia is crucial. Two subtypes of sporadic gastric cancer have been recognized: cardia subtype and non-cardia (distal) subtype, the latter being more frequent and largely associated with infection of Helicobacter pylori, a class I carcinogen. Helicobacter pylori initiates the widely accepted Correa cascade, describing a stepwise progression through precursor lesions from chronic inflammation to gastric atrophy, gastric intestinal metaplasia and neoplasia. Our knowledge on He-licobacter pylori is still limited, and multiple questions in the context of its contribution to the pathogenesis of gastric neoplasia are yet to be answered. Awareness and recognition of gastric atrophy and intestinal metaplasia on high-definition white-light endoscopy, image-enhanced endoscopy and magnification endoscopy, in combination with histology from the biopsies taken accurately according to the protocol, are crucial to guiding the management. Standard indications for endoscopic resections (endoscopic mucosal resection and endoscopic submucosal dissection) of gastric dysplasia and intestinal type of gastric carcinoma have been recommended by multiple societies. Endoscopic evaluation and surveillance should be offered to individuals with an inherited predisposition to gastric carcinoma.

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Molecular Mechanism of Helicobacter pylori-Induced Gastric Cancer

Cited by 154 publications

References 102 publications

Biofilm Formation as a Complex Result of Virulence and Adaptive Responses of Helicobacter pylori

Biofilm Formation as a Complex Result of Virulence and Adaptive Responses of Helicobacter pylori

Peripheral Cytokine Levels as a Prognostic Indicator in Gastric Cancer: A Review of Existing Literature

Advances in the Aetiology & Endoscopic Detection and Management of Early Gastric Cancer

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