ArticleHelicobacter2008
H. pylori-induced apoptosis in human gastric cancer cells mediated via the release of apoptosis-inducing factor from mitochondria.
Article in Helicobacter, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 44 citations in OpenAlex.
- There Are No Insurmountable Barriers: Passage of theMembranes · 2023Review
- CMTM3 protects the gastric epithelial cells from apoptosis and promotes IL-8 by stabilizing NEMO during Helicobacter pylori infection.Gut pathogens · 2023Article
- Review
- Investigation ofFrontiers in microbiology · 2023Article
- Article
- Crohn's Disease Pathobiont Adherent-Invasive E coli Disrupts Epithelial Mitochondrial Networks With Implications for Gut Permeability.Cellular and molecular gastroenterology and hepatology · 2021Article
- Helicobacter pylori outer membrane vesicles involvement in the infection development and Helicobacter pylori-related diseases.Journal of biomedical science · 2018Review
- Binding of the Helicobacter pylori OipA causes apoptosis of host cells via modulation of Bax/Bcl-2 levels.Scientific reports · 2017Article
- Article
- Bid-Induced Release of AIF/EndoG from Mitochondria Causes Apoptosis of Macrophages during Infection withFrontiers in cellular and infection microbiology · 2017Article
- Role of Helicobacter pylori infection in pathogenesis of gastric carcinoma.World journal of gastrointestinal pathophysiology · 2016Review
- NaCl pretreatment attenuates H.pylori-induced DNA damage and exacerbates proliferation of gastric epithelial cells (GES-1).Infectious agents and cancer · 2015Article
- Effect of Helicobacter pylori on gastric epithelial cells.World journal of gastroenterology · 2014Review
- The expression of Bcl-2 and BID in gastric cancer cells.Journal of immunology research · 2014Article
- Helicobacter pylori protection against reflux esophagitis.Digestive diseases and sciences · 2012Article
- Role of apoptosis-inducing factor, proline dehydrogenase, and NADPH oxidase in apoptosis and oxidative stress.Cell health and cytoskeleton · 2012Article
- The 19 kDa Mycobacterium tuberculosis lipoprotein (LpqH) induces macrophage apoptosis through extrinsic and intrinsic pathways: a role for the mitochondrial apoptosis-inducing factor.Clinical & developmental immunology · 2012Article
- Down-regulation of HSP70 sensitizes gastric epithelial cells to apoptosis and growth retardation triggered by H. pylori.BMC gastroenterology · 2011Article
- Helicobacter pylori vacuolating toxin A and apoptosis.Cell communication and signaling : CCS · 2011Article
- Helicobacter pylori VacA toxin/subunit p34: targeting of an anion channel to the inner mitochondrial membrane.PLoS pathogens · 2010Article
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 2 countries.
Funding
Abstract
BACKGROUND AND
aimOur previous study of Helicobacter pylori-induced apoptosis showed the involvement of Bcl-2 family proteins and cytochrome c release from mitochondria. Here, we examine the release of other factors from mitochondria, such as apoptosis-inducing factor (AIF), and upstream events involving caspase-8 and Bid.
methodsHuman gastric adenocarcinoma (AGS) cells were incubated with a cagA-positive H. pylori strain for 0, 3, 6, and 24 hours and either total protein or cytoplasmic, nuclear, and mitochondrial membrane fractions were collected.
resultsProteins were immunoblotted for AIF, Bid, polyadenosine ribose polymerase (PARP), caspase-8, and beta-catenin. H. pylori activated caspase-8, caused PARP cleavage, and attenuated mitochondrial membrane potential. A time-dependent decrease in beta-catenin protein expression was detected in cytoplasmic and nuclear extracts, coupled with a decrease in beta-actin. An increase in the cytoplasmic pool of AIF was seen as early as 3 hours after H. pylori exposure, and a concomitant increase was seen in nuclear AIF levels up to 6 hours. A band corresponding to full-length Bid was seen in both the cytoplasmic and the nuclear fractions of controls, but not after H. pylori exposure. Active AIF staining was markedly increased in gastric mucosa from infected persons, compared to uninfected controls.
conclusionH. pylori might trigger apoptosis in AGS cells via interaction with death receptors in the plasma membrane, leading to the cleavage of procaspase-8, release of cytochrome c and AIF from mitochondria, and activation of subsequent downstream apoptotic events, as reported previously for chlorophyllin. This is consistent with AIF activation that was found in the gastric mucosa of humans infected with H. pylori. Hence, the balance between apoptosis and proliferation in these cells may be altered in response to injury caused by H. pylori infection, leading to an increased risk of cancer.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.