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. 2023 Mar 23;15(1):2192501. doi: 10.1080/19490976.2023.2192501

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© 2023 The Author(s). Published with license by Taylor & Francis Group, LLC.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The terms on which this article has been published allow the posting of the Accepted Manuscript in a repository by the author(s) or with their consent.

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Figure 8. — Working models of the crosstalk between the YAP and β-catenin pathways in H. pylori-induced gastric tumorigenesis. H. pylori infection invades the gastric epithelium and induces nuclear accumulation and transcriptional activation of YAP and β-catenin. Mechanistically, YAP interacts with β-catenin and promotes its nuclear activation. As a result, their common target genes, including CDX2, LGR5 and RUVBL1, are activated, which contributes to cell proliferation and expansion, ultimately leading to gastric carcinogenesis.