ArticleCancer medicine2020
Helicobacter pylori infection leads to KLF4 inactivation in gastric cancer through a TET1-mediated DNA methylation mechanism.
Article in Cancer medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 54 citations in OpenAlex.
- Advances inOncology letters · 2026Review
- KLF family of proteins in gastrointestinal tumors (Review).Oncology letters · 2026Review
- Hijacked epigenomes: how bacterial effectors rewrite host gene expression.Archives of microbiology · 2026Review
- Krüppel-Like Factor 4, a Hub Gate for Cell Crosstalk in Tumor Microenvironment.Cancer medicine · 2026Review
- Myeloid-derived suppressor cells modulation in the context of tumor microenvironment for gastric cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025Review
- Aberrant DNA methylation and overexpression of NR0B1 are prognostic biomarkers in KEAP1-mutant lung adenocarcinomas.Discover oncology · 2025Article
- Microbiota-driven epigenetic modifications in gastrointestinal cancer: Implications for pathogenesis and therapeutic strategies.World journal of microbiology & biotechnology · 2025Review
- Mechanism of KLF4 Inhibition of epithelial-mesenchymal transition in gastric cancer cells.Open life sciences · 2025Article
- KLF4: a multifunctional nexus connecting tumor progression and immune regulation.Frontiers in immunology · 2025Review
- LINC01089 in cancer: multifunctional roles and therapeutic implications.Journal of translational medicine · 2024Review
- Helicobacter pylori-induced aberrant demethylation and expression of GNB4 promotes gastric carcinogenesis via the Hippo-YAP1 pathway.BMC medicine · 2023Article
- Transcription factor CASZ1 increases an oncogenic transcriptional process in tumorigenesis and progression of glioma cells.MedComm · 2022Article
- SAMHD1, positively regulated by KLF4, suppresses the proliferation of gastric cancer cells through MAPK p38 signaling pathway.Cell cycle (Georgetown, Tex.) · 2022Article
- Increased 5-hydroxymethylcytosine is a favorable prognostic factor ofWorld journal of gastrointestinal oncology · 2022Article
- Performance of DNA Methylation on the Molecular Pathogenesis ofJournal of pharmacopuncture · 2022Review
- SMYD2 aggravates gastrointestinal stromal tumor via upregulation of EZH2 and downregulation of TET1.Cell death discovery · 2022Article
- Emerging Role ofFrontiers in oncology · 2022Review
- Association betweenPeerJ · 2022Article
- Current research advances in microRNA-mediated regulation of Krüppel-like factor 4 in cancer: a narrative review.Annals of translational medicine · 2021Review
- MicroRNA-21 from bone marrow mesenchymal stem cell-derived extracellular vesicles targets TET1 to suppress KLF4 and alleviate rheumatoid arthritis.Therapeutic advances in chronic disease · 2021Article
Corrections and comments
- Erratum issued
Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Krüppel-like factor 4 (KLF4) has a tumor suppressor role in the progression of gastric cancer (GC), and inhibition or loss of KLF4 expression was identified in GC. The aim of this study was to explore the new molecular mechanism of KLF4 inactivation in gastric cancer. Herein, we report that Helicobacter pylori infection or Cag pathogenicity island protein A (CagA) gene transduction resulted in KLF4 expression downregulation and promoted gastric epithelial cell and gastric cancel cell proliferation, migration, and colony formation. Mechanistically, we found that CagA gene transduction led to DNA methylation of the KLF4 promoter, an effect that was relevant to the significant downregulation of TET1 expression. Causally, knockdown of TET1 expression decreased KLF4 expression, whereas overexpression of TET1 had the opposite effect. Clinically, we found that KLF4 expression and the 5-hmC levels were lower in GC cells with H pylori infection than in GC cells without H pylori infection. Thus, our study not only sheds new light on how H pylori infection promotes the progression of GC but also elucidates a novel mechanism of KLF4 inactivation in GC pathogenesis. During pathogenesis, an alteration in the H pylori/CagA-TET1-KLF4 signaling pathway plays a critical role, suggesting that this pathway may be a prospective target for gastric carcinoma intervention and therapy.
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