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. 2018 Nov 22;37:280. doi: 10.1186/s13046-018-0962-5

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© The Author(s). 2018

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Fig. 8 — The proposed mechanism of H. pylori CagA-mediated promotion of gastric tumorigenesis. CagA⁺ H. pylori delivers CagA into gastric epithelial cells via T4SS where CagA induces oncogene YAP expression, increases nuclear translocation of YAP that elevates downstream gene expression. The H. pylori CagA-mediated activation of YAP then leads to enhanced EMT program, thereby further promoting gastric tumorigenesis