ArticleThe Journal of clinical investigation2020
Bacterial CagA protein compromises tumor suppressor mechanisms in gastric epithelial cells.
Article in The Journal of clinical investigation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
37 citing papers in PubMed, 55 citations in OpenAlex.
- Lineage-Specific CagA Binding Mechanics and Microenvironmental Rewiring in East Asian Gastric Carcinogenesis.Molecules (Basel, Switzerland) · 2026Article
- C2ORF68 stabilizes SIVA1 to upregulate BCL-2 and suppress apoptosis in gallbladder cancer.Cell death discovery · 2026Article
- Helicobacter pylori activates the TRAF1/OASL/ZBP1-PANoptosome pathway to induce PANoptosis in the gastric mucosa.Apoptosis : an international journal on programmed cell death · 2026Article
- Bacterial contributions to cancer development: mechanisms, dysbiosis, and cross-cancer associations.Infectious agents and cancer · 2026Review
- AhR Activation Transcriptionally Induces Anti-Microbial Peptide Alpha-Defensin 1 Leading to Reversal of Gut Microbiota Dysbiosis and Colitis.Gut microbes · 2025Article
- Gut microbiome and gastric cancer: microbial interactions and therapeutic potential.Gut pathogens · 2025Review
- Helicobacter pylori is associated with less tumor-infiltrating lymphocytes and a poor prognosis in gastric cancer.BMC gastroenterology · 2025Article
- Helicobacter pylori CagA elevates FTO to induce gastric cancer progression via a "hit-and-run" paradigm.Cancer communications (London, England) · 2025Article
- Review
- The role of oral microbiota in digestive system diseases: current advances and perspectives.Journal of oral microbiology · 2025Review
- H. Pylori-Facilitated TERT/Wnt/β-Catenin Triggers Spasmolytic Polypeptide-Expressing Metaplasia and Oxyntic Atrophy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Decoding microbial carcinogenic strategies: ubiquitination and SUMO modification.Frontiers in microbiology · 2025Review
- Potential mechanism of traditional Chinese medicine intervention in gastric cancer: targeted regulation of autophagy.Frontiers in pharmacology · 2025Review
- An antibiotic-free platform for eliminating persistentActa pharmaceutica Sinica. B · 2024Article
- Sustained exposure to Helicobacter pylori induces immune tolerance by desensitizing TLR6.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2024Article
- Helicobacter pylori CagA-mediated ether lipid biosynthesis promotes ferroptosis susceptibility in gastric cancer.Experimental & molecular medicine · 2024Article
- The Most Recent Insights into the Roots of Gastric Cancer.Life (Basel, Switzerland) · 2024Review
- Interaction between intestinal flora and gastric cancer in tumor microenvironment.Frontiers in oncology · 2024Review
- PPARδ dysregulation of CCL20/CCR6 axis promotes gastric adenocarcinoma carcinogenesis by remodeling gastric tumor microenvironment.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2023Article
- Research progress on exosomal proteins as diagnostic markers of gastric cancer (review article).Clinical and experimental medicine · 2023Review
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8 authors at 3 institutions in 1 country.
Funding
Abstract
Approximately half of the world's population is infected with the stomach pathogen Helicobacter pylori. Infection with H. pylori is the main risk factor for distal gastric cancer. Bacterial virulence factors, such as the oncoprotein CagA, augment cancer risk. Yet despite high infection rates, only a fraction of H. pylori-infected individuals develop gastric cancer. This raises the question of defining the specific host and bacterial factors responsible for gastric tumorigenesis. To investigate the tumorigenic determinants, we analyzed gastric tissues from human subjects and animals infected with H. pylori bacteria harboring different CagA status. For laboratory studies, well-defined H. pylori strain B128 and its cancerogenic derivative strain 7.13, as well as various bacterial isogenic mutants were employed. We found that H. pylori compromises key tumor suppressor mechanisms: the host stress and apoptotic responses. Our studies showed that CagA induces phosphorylation of XIAP E3 ubiquitin ligase, which enhances ubiquitination and proteasomal degradation of the host proapoptotic factor Siva1. This process is mediated by the PI3K/Akt pathway. Inhibition of Siva1 by H. pylori increases survival of human cells with damaged DNA. It occurs in a strain-specific manner and is associated with the ability to induce gastric tumor.
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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.