ArticleCancer communications (London, England)2025
Helicobacter pylori CagA elevates FTO to induce gastric cancer progression via a "hit-and-run" paradigm.
Article in Cancer communications (London, England), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed.
- The role, regulatory mechanisms, and therapeutic implications of FTO in gastrointestinal cancer.Genes & diseases · 2026Review
- The evolving landscape of the Warburg effect in gastric cancer: From molecular mechanisms to targeted therapy.Clinical and translational medicine · 2026Review
- Integrative multi-omics, machine learning, and experimental validation reveal that TPM1 suppresses M2 macrophage polarization and enhances chemosensitivity in acute myeloid leukemia.Cell biology and toxicology · 2026Article
- Emerging roles of RNA mInternational journal of oncology · 2026Review
- RNA mCell biology and toxicology · 2026Review
- Decoupling ecological and pathogenic roles: Helicobacter pylori as a gastric hegemon maintaining order or amplifying dysbiotic chaos.FEMS microbiology letters · 2026Article
- Deciphering intratumoral microbiota in digestive system tumors: mechanisms and emerging therapeutic strategies.Frontiers in cellular and infection microbiology · 2026Review
- Reader-dependent functional duality of FTO: a context-switching node at the intersection of immune evasion and therapeutic resistance.Frontiers in immunology · 2026Review
- The interplay of the microbiome, host genetics, and epigenetic modifications in gastric cancer.Frontiers in microbiology · 2026Review
- From Tumor Biology to Clinical Perspectives: Novel Biomarkers and Therapeutic Insights in Gastric Cancer.Oncology research · 2026Review
- The association of the advanced lung cancer inflammation index with the risk ofFrontiers in cellular and infection microbiology · 2026Article
- TK1 in gastric cancer: Helicobacter pylori-driven oncogenesis biomarker, utility, and emerging targeted therapies.Frontiers in oncology · 2026Review
- Organoid models: applications and research advances in gastric cancer.Frontiers in oncology · 2026Review
- Epitranscriptomic modifications in programmed cell death: mechanistic insights and implications for liver diseases.Cellular & molecular biology letters · 2025Review
- Gastrointestinal microbiota in treatment of gastric precancerous lesions and gastric cancer by Western and traditional Chinese medicine.World journal of clinical oncology · 2025Review
- Article
- Review
- Helicobacter pylori CagA elevates FTO to induce gastric cancer progression via a "hit-and-run" paradigm.Cancer communications (London, England) · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
Abstract
backgroundHelicobacter pylori (H. pylori) infection contributes significantly to gastric cancer (GC) progression. The intrinsic mechanisms of H. pylori-host interactions and their role in promoting GC progression need further investigation. In this study, we explored the potential role of fat mass and obesity-associated protein (FTO) in mediating Cytotoxin-associated gene A (CagA)-induced GC progression.
methodsThe effects of H. pylori infection on N
resultsInfection with cagA-positive H. pylori upregulated the expression of FTO, which was essential for CagA-mediated GC metastasis and significantly associated with a poor prognosis in GC patients. Mechanistically, CagA delivered by H. pylori enhanced FTO transcription via Jun proto-oncogene. Elevated FTO induced demethylation of m
conclusionOur study revealed that FTO mediates the "hit-and-run" mechanism of CagA-induced GC progression, which suggests that the therapeutic targeting of FTO could offer a promising approach to the prevention of CagA-induced cancer progression.
Indexed as
Identifiers
What OpenQuestion holds
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.