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. 2019 Jun 10;11(6):801. doi: 10.3390/cancers11060801

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© 2019 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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Schematic illustration depicting how the Helicobacter pylori (H. pylori) virulence factor gamma-glutamyltranspeptidase (HpGGT) acts upon infection of gastric (AGS and GES-1) cells. HpGGT is secreted and is shown to inhibit gastric cell autophagy (1–6) and, in the case of AGS cells, to do so by reducing levels of the lysosomal cysteine protease Cathepsin B. H. pylori is suggested in these cells to increase lysosomal membrane permeability to favor Cathepsin B leakage (4), thereby impairing lysosome degradation upon fusion with the autophagosome (5). In parallel, HpGGT is depicted as being necessary for H. pylori internalization (7) by gastric (AGS and GES-1) cells and thus as a virulence factor that facilitates bacterial invasion of gastric cells.