Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2023 Aug 6;9(8):e18945.
doi: 10.1016/j.heliyon.2023.e18945. eCollection 2023 Aug.

Helicobacter pylori and epithelial mesenchymal transition in human gastric cancers: An update of the literature

Affiliations
Review

Helicobacter pylori and epithelial mesenchymal transition in human gastric cancers: An update of the literature

Tala M Jamal Eddin et al. Heliyon. .

Abstract

Gastric cancer, a multifactorial disease, is considered one of the most common malignancies worldwide. In addition to genetic and environmental risk factors, infectious agents, such as Epstein-Barr virus (EBV) and Helicobacter pylori (H.pylori) contribute to the onset and development of gastric cancer. H. pylori is a type I carcinogen that colonizes the gastric epithelium of approximately 50% of the world's population, thus increasing the risk of gastric cancer development. On the other hand, epithelial mesenchymal transition (EMT) is a fundamental process crucial to embryogenic growth, wound healing, organ fibrosis and cancer progression. Several studies associate gastric pathogen infection of the epithelium with EMT initiation, provoking cancer metastasis in the gastric mucosa through various molecular signaling pathways. Additionally, EMT is implicated in the progression and development of H. pylori-associated gastric cancer. In this review, we recapitulate recent findings elucidating the association between H. pylori infection in EMT promotion leading to gastric cancer progression and metastasis.

Keywords: Cancer progression; Epithelial–mesenchymal transition; Gastric cancer; H.pylori.

PubMed Disclaimer

Conflict of interest statement

“The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript, or in the decision to publish the results”.

Figures

Fig. 1
Fig. 1
Phenotypic alterations involving loss of epithelial cell characteristics (orange to green color) and its transition to the mesenchymal cell phenotype (green color). The orange color symbolizes the characteristics of epithelial cells, which typically exhibit strong cell-cell adhesion, organized cellular morphology, and a polarized structure. These cells are associated with the maintenance of tissue integrity and specialized functions. As the color transitions from orange to green, it represents the phenotypic changes occurring during the epithelial-to-mesenchymal transition (EMT). This transition involves a loss of epithelial traits and the acquisition of mesenchymal ones, characterized by decreased cell-cell adhesion, a more elongated and spindle-shaped morphology, enhanced migratory capabilities, and increased production of extracellular matrix components.
Fig. 2
Fig. 2
H. pylori induced signaling pathways to stimulate the onset and development of cancer. The figure illustrates the intricate signaling pathways induced by Helicobacter pylori (H.pylori) infection, which play a pivotal role in promoting the initiation and progression of cancer. The figure highlights several key events initiated by H. pylori, starting with its adherence and colonization to gastric epithelial cells. This leads to the activation of inflammatory signaling pathways, including NF-κB, MAPK, and JAK/STAT, resulting in the production of pro-inflammatory cytokines, chemokines, and reactive oxygen species. The chronic inflammation caused by H. pylori infection subsequently triggers DNA damage and genetic alterations in gastric epithelial cells. Concurrently, H. pylori stimulates cell proliferation and survival pathways, such as PI3K/Akt and Ras/Raf/MAPK, promoting uncontrolled cell growth and resistance to apoptosis.

Similar articles

Cited by

References

    1. Machlowska J., et al. Gastric cancer: epidemiology, risk factors, classification, genomic characteristics and treatment strategies. Int. J. Mol. Sci. 2020;21:E4012. doi: 10.3390/ijms21114012. - DOI - PMC - PubMed
    1. Van Cutsem E., et al. Gastric cancer. Lancet. 2016;388(10060):2654–2664. doi: 10.1016/S0140-6736(16)30354-3. - DOI - PubMed
    1. Sitarz R., et al. Gastric cancer: epidemiology, prevention, classification, and treatment. Cancer Manag. Res. 2018;10:239–248. - PMC - PubMed
    1. Hartgrink H.H., et al. Gastric cancer. Lancet. 2009;374(9688):477–490. - PMC - PubMed
    1. Smyth E.C., et al. Gastric cancer. Lancet. 2020;396(10251):635–648. - PubMed

LinkOut - more resources

  NODES
Association 2
twitter 2