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Review
. 2015 Nov 3;6(34):35579-88.
doi: 10.18632/oncotarget.5758.

Wnt/β-catenin, an oncogenic pathway targeted by H. pylori in gastric carcinogenesis

Affiliations
Review

Wnt/β-catenin, an oncogenic pathway targeted by H. pylori in gastric carcinogenesis

Xiaowen Song et al. Oncotarget. .

Abstract

A section of gastric cancers presents nuclear β-catenin accumulation correlated with H. pylori infection. H. pylori stimulate Wnt/β-catenin pathway by activating oncogenic c-Met and epidermal growth factor receptor (EGFR), or by inhibiting tumor suppressor Runx3 and Trefoil factor 1 (TFF1). H. pylori also trigger Wnt/β-catenin pathway by recruiting macrophages. Moreover, Wnt/β-catenin pathway is found involved in H. pylori-induced gastric cancer stem cell generation. Recently, by using gastroids, researchers have further revealed that H. pylori induce gastric epithelial cell proliferation through β-catenin. These findings indicate that Wnt/β-catenin is an oncogenic pathway activated by H. pylori. Therefore, this pathway is a potential therapy target for H. pylori-related gastric cancer.

Keywords: Helicobacter pylori; Wnt; gastric cancer; β-catenin.

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Conflict of interest statement

CONFLICTS OF INTEREST

There is no financial conflict of interest concerning this study.

Figures

Figure 1
Figure 1. Wnt/β-catenin signal pathway
Upon the binding of Wnt proteins to their receptors, β-catenin dissociates from its degrading complex, which consists of scaffold protein AXIN, casein kinase 1α (CK1α), tumor suppressor adenomatous polyposis coli (APC), and glycogen synthase kinase 3β (GSK3β). The accumulated β-catenin in cytoplasm then translocates into nucleus. P: Phosphorylation.
Figure 2
Figure 2. The mechanisms underlying gastric carcinogenesis induced by H. pylori
The mechanisms include chronic inflammation in gastric mucosa, genetic and epigenetic alterations of tumor suppressor genes, activation of oncogenic signals, and generation of gastric cancer stem cells (CSC).
Figure 3
Figure 3. Intracellular signalings mediating the activation of Wnt/β-catenin by H. pylori
Methyl: methylation.

References

    1. Logan CY, Nusse R. The Wnt signaling pathway in development and disease. Annu Rev Cell Dev Biol. 2004;20:781–810. - PubMed
    1. Clevers H. Wnt/beta-catenin signaling in development and disease. Cell. 2006;127:469–480. - PubMed
    1. Hanahan D, Weinberg RA. Hallmarks of cancer: the next generation. Cell. 2011;144:646–674. - PubMed
    1. Diakos CI, Charles KA, McMillan DC, Clarke SJ. Cancer-related inflammation and treatment effectiveness. Lancet Oncol. 2014;15:e493–503. - PubMed
    1. Tu S, Bhagat G, Cui G, Takaishi S, Kurt-Jones EA, Rickman B, Betz KS, Penz-Oesterreicher M, Bjorkdahl O, Fox JG, Wang TC. Overexpression of interleukin-1beta induces gastric inflammation and cancer and mobilizes myeloid-derived suppressor cells in mice. Cancer Cell. 2008;14:408–419. - PMC - PubMed

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