Human gastric fibroblasts ameliorate A20-dependent cell survival in co-cultured gastric epithelial cells infected by Helicobacter pylori

Cortactin-dependent control of Par1b-regulated epithelial cell polarity in Helicobacter infection

“…In particular, we observed more prominent Par1b staining in the apical compartments of non-infected gastric mucosoids as compared to non-infected Caco-2 monolayers. These differences could be explained by the mucus layer produced in gastric mucosoids, which is less pronounced in Caco-2 cells ( Jantaree et al., 2022 ; Navabi et al., 2013 ). Mucin production was shown to be connected to cell polarity, which could potentially affect Par1b distribution closer to the apical side ( Kufe, 2009 ).…”

“…Mucosoid cultures between passages 5–20 were used for experiments. Gastric mucosoids were cultured as described previously ( Jantaree et al., 2022 ). In brief, 4 × 10 5 cells derived from gastric organoids were seeded onto a collagen-coated (15 μg/cm 2 , A10644-01, Gibco®) membrane of a 12-well ThinCert™ insert.…”

Research Progress for Targeting Deubiquitinases in Gastric Cancers

“…Intriguingly, three studies discovered that non-coding RNAs are also key mediators of interactions between GC cells and other cell types, including gastric mucosa cells, CAFs, and M2-polarized macrophages, and that USP3, USP7, and CYLD are linked to this process [ 24 , 27 , 76 ]. Furthermore, several infectious agents, cytokines, and antitumor agents also affect the expression of several DUBs, such as USP3, USP7, USP10, USP29, CYLD, and A20 [ 21 , 27 , 32 , 54 , 73 , 97 , 98 , 122 ] ( Table 1 ), which implicates unknown pro-cancer effects under certain circumstances.…”

“…Moreover, the DUB activity of A20 counteracted the ubiquitination of procaspase-8, thereby restricting caspase-8 activity and apoptosis [ 96 ]. Consistently, NF-κB activation induced A20 upregulation during H. pylori infection, mainly because USP48 stabilizes nuclear RelA and promotes its transcriptional activity [ 95 , 96 , 97 , 98 ]. Together, USP48 and A20 promoted GC cell survival during H. pylori infection and suggested an oncogenic role for A20.…”