ArticleWorld journal of microbiology & biotechnology2021
Regulation of β1-integrin in autophagy and apoptosis of gastric epithelial cells infected with Helicobacter pylori.
Article in World journal of microbiology & biotechnology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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7 citing papers in PubMed, 6 citations in OpenAlex.
- Loss of L1CAM from gastric epithelial cells and extracellular vesicles promotes Helicobacter pylori-driven cancer progression and invasiveness.Cell communication and signaling : CCS · 2026Article
- The dual role of gastric microbiota dysbiosis in gastric cancer progression and therapy.International journal of clinical oncology · 2026Review
- Knocking Down HN1 Blocks Helicobacter pylori-Induced Malignant Phenotypes in Gastric Mucosal Cells and Inhibits Gastric Cancer Cell Proliferation, Cytoskeleton Remodeling, and Migration.Biochemical genetics · 2025Article
- Helicobacter pylori and gastric cancer: mechanisms and new perspectives.Journal of hematology & oncology · 2025Review
- Eliminating the invading extracellular and intracellular FnBpFrontiers in cellular and infection microbiology · 2023Article
- Overexpression of integrin βAnnals of translational medicine · 2022Article
- β1-Integrin plays a major role in resveratrol-mediated anti-invasion effects in the CRC microenvironment.Frontiers in pharmacology · 2022Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Helicobacter pylori infection is an essential factor in the development of human gastric diseases, but its pathogenic mechanism is still unclear. In this work we have showed that, the LC3II levels were increased and β1-integrin levels were decreased in H. pylori-positive human gastric tissue samples and H. pylori co-cultured GES-1 cells. There was significant upregulation of LC3II levels and downregulation of P62 levels in GES-1 cells after β1-integrin knockdown co-cultured with H. pylori. This indicated that β1-integrin downregulation promoted autophagy in GES-1 cells after H. pylori infection. The cell apoptosis rate and poly ADP-ribose polymerase (PARP) and caspase-3 activities were increased in GES-1 cells pretreated with 3-methyladenine (3-MA ) after H. pylori infection. Furthermore, there was a significant decrease in apoptosis of β1-integrin knockdown GES-1 cells co-cultured with H. pylori; apoptosis was also downregulated in β1-integrin knockdown- and 3-MA-treated GES-1 cells co-cultured with H. pylori. Correspondingly, PARP and caspase-3 activities were decreased in β1-integrin knockdown cells co-cultured with H. pylori and β1-integrin knockdown-3-MA-treated-1 cells with H. pylori infection. Thus, β1-integrin is a novel autophagy and apoptosis regulator during H. pylori infection. However, inhibition of autophagy did not reverse the decrease in apoptosis caused by downregulation of β1-integrin.
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