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Peer-reviewedCC BY 4.0Frontiers in Immunology

The STAT1 lexicon: translating signaling codes in H. pylori-driven gastric carcinogenesis

  • Wei Han1,2
  • Hongzheng He3
  • Bei Ye4
  • Yilin Sun4
  • XiuPing Wang4
  • Tingting Liu5
  • Hanwei Cui6
  • Jianjun Wang4
6 affiliations
  1. 1Science and Education Department, Kunshan Maternity and Children’s Health Care Hospital
  2. 2Department of General Surgery, Kunshan Hospital Affiliated to Jiangsu University
  3. 3Department of Clinical Laboratory, Jinxi People’s Hospital of Kunshan
  4. 4Department of Clinical Laboratory, Kunshan Hospital Affiliated to Jiangsu University
  5. 5Science and Technology Talent Department, Kunshan Hospital Affiliated to Jiangsu University
  6. 6Central Laboratory, The Fourth People’s Hospital of Shenzhen
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Abstract

Helicobacter pylori ( H. pylori ) is a chronic gastric mucosa colonizer that leads to the Correa cascade of gastric adenocarcinoma progression: chronic gastritis, intestinal metaplasia, and dysplasia. Signal transducer and activator of transcription 1 (STAT1) is one of the key mediators at the host immunity-tumor cell interface. The interaction of H. pylori with pattern recognition receptors on gastric epithelial cells induces tyrosine phosphorylation of STAT1 by Janus kinase (JAK), which in turn leads to dimerization and nuclear translocation of the protein, resulting in the suppression of pathogen survival enabled by interferon (IFN)-regulatory transcriptional programs. Ironically, STAT1 has a dual role in gastric carcinogenesis in a context-dependent manner: in the early disease, it acts as a tumor suppressor by facilitating apoptosis and cell-cycle arrest in gastric lesions, but in the advanced disease, it plays a role in immune evasion and tumor progression through the expression of programed death-ligand 1 (PD-L1) and tumor microenvironment (TME) modulation. This review critically assesses how H. pylori manipulates the STAT1 signaling during the infection process, crosstalk between the STAT1 and STAT3 pathways, and the future use of this understanding to therapeutically target and develop biomarkers. New strategies such as small-molecule STAT inhibitors, combination immunotherapy, and artificial intelligence (AI)-based biomarker discovery are discussed, as well as existing limitations and future research directions.

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Cite

BibTeXRIS
BibTeX
@article{han2026stat1,
  title = {{The STAT1 lexicon: translating signaling codes in H. pylori-driven gastric carcinogenesis}},
  author = {Wei Han and Hongzheng He and Bei Ye and Yilin Sun and XiuPing Wang and Tingting Liu and Hanwei Cui and Jianjun Wang},
  journal = {Frontiers in Immunology},
  year = {2026},
  month = oct,
  doi = {10.3389/fimmu.2026.1679212},
  url = {https://www.frontiersin.org/articles/10.3389/fimmu.2026.1679212/full},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - The STAT1 lexicon: translating signaling codes in H. pylori-driven gastric carcinogenesis
AU  - Wei Han
AU  - Hongzheng He
AU  - Bei Ye
AU  - Yilin Sun
AU  - XiuPing Wang
AU  - Tingting Liu
AU  - Hanwei Cui
AU  - Jianjun Wang
PY  - 2026
DA  - 2026/10/22
JO  - Frontiers in Immunology
DO  - 10.3389/fimmu.2026.1679212
UR  - https://www.frontiersin.org/articles/10.3389/fimmu.2026.1679212/full
AB  - Helicobacter pylori ( H. pylori ) is a chronic gastric mucosa colonizer that leads to the Correa cascade of gastric adenocarcinoma progression: chronic gastritis, intestinal metaplasia, and dysplasia. Signal transducer and activator of transcription 1 (STAT1) is one of the key mediators at the host immunity-tumor cell interface. The interaction of H. pylori with pattern recognition receptors on gastric epithelial cells induces tyrosine phosphorylation of STAT1 by Janus kinase (JAK), which in turn leads to dimerization and nuclear translocation of the protein, resulting in the suppression of pathogen survival enabled by interferon (IFN)-regulatory transcriptional programs. Ironically, STAT1 has a dual role in gastric carcinogenesis in a context-dependent manner: in the early disease, it acts as a tumor suppressor by facilitating apoptosis and cell-cycle arrest in gastric lesions, but in the advanced disease, it plays a role in immune evasion and tumor progression through the expression of programed death-ligand 1 (PD-L1) and tumor microenvironment (TME) modulation. This review critically assesses how H. pylori manipulates the STAT1 signaling during the infection process, crosstalk between the STAT1 and STAT3 pathways, and the future use of this understanding to therapeutically target and develop biomarkers. New strategies such as small-molecule STAT inhibitors, combination immunotherapy, and artificial intelligence (AI)-based biomarker discovery are discussed, as well as existing limitations and future research directions.
SN  - 1664-3224
ER  -