ArticlePloS one2019
KLF4 activates NFκB signaling and esophageal epithelial inflammation via the Rho-related GTP-binding protein RHOF.
Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 29 citations in OpenAlex.
- Analysis of Allele-Specific Expression Highlights Novel Participants of Empagliflozin-Driven Effects on T2DM-Associated Regulatory Pathways.International journal of molecular sciences · 2026Article
- KCTD15 Enhances Stem Cell-Like Properties and Promotes Triple-Negative Breast Cancer Progression Through KLF4/β-Catenin Signaling.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- ALK5 inhibition reduces HDM-induced inflammation and oxidative injury by regulating KLF4-mediated glycolysis in BEAS-2B cells.Journal of bioenergetics and biomembranes · 2026Article
- Decoding Rho GTPase signalling networks in directed cell migration.Frontiers in cell and developmental biology · 2026Review
- Review
- MiR-7a-Klf4 axis as a regulator and therapeutic target of neuroinflammation and ferroptosis in Alzheimer's disease.NAR molecular medicine · 2025Article
- The protective effect of iron isomaltoside on myocardial ischemia-reperfusion injury via the suppression of KLF4/NF-κB signaling.PloS one · 2025Article
- RHOF promotes Snail1 lactylation by enhancing PKM2-mediated glycolysis to induce pancreatic cancer cell endothelial-mesenchymal transition.Cancer & metabolism · 2024Article
- KLF4 Induces Colorectal Cancer by Promoting EMT via STAT3 Activation.Digestive diseases and sciences · 2024Article
- RHOF activation of AKT/β-catenin signaling pathway drives acute myeloid leukemia progression and chemotherapy resistance.iScience · 2024Article
- The Kruppel-like factor 4-signal transducer and activator of transcription 5A axis promotes pancreatic fibrosis in mice with caerulein-induced chronic pancreatitis.Experimental animals · 2023Article
- KLF4 transcription factor in tumorigenesis.Cell death discovery · 2023Review
- Krüppel-like factors in tumors: Key regulators and therapeutic avenues.Frontiers in oncology · 2023Review
- Determining the immune environment of cutaneous T-cell lymphoma lesions through the assessment of lesional blood drops.Scientific reports · 2021Article
- Extrachromosomal circular DNAs are common and functional in esophageal squamous cell carcinoma.Annals of translational medicine · 2021Article
- Temporal multiomic modeling reveals a B-cell receptor proliferative program in chronic lymphocytic leukemia.Leukemia · 2021Article
- Review
- High Expression of RhoF Predicts Worse Overall Survival: A Potential Therapeutic Target for non-M3 Acute Myeloid Leukemia.Journal of Cancer · 2021Article
- Identification of an N6-methyladenosine-mediated positive feedback loop that promotes Epstein-Barr virus infection.The Journal of biological chemistryArticle
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
Understanding the regulatory mechanisms within esophageal epithelia is essential to gain insight into the pathogenesis of esophageal diseases, which are among the leading causes of morbidity and mortality throughout the world. The zinc-finger transcription factor Krüppel-like factor (KLF4) is implicated in a large number of cellular processes, such as proliferation, differentiation, and inflammation in esophageal epithelia. In murine esophageal epithelia, Klf4 overexpression causes chronic inflammation which is mediated by activation of NFκB signaling downstream of KLF4, and this esophageal inflammation produces epithelial hyperplasia and subsequent esophageal squamous cell cancer. Yet, while NFκB activation clearly promotes esophageal inflammation, the mechanisms by which NFκB signaling is activated in esophageal diseases are not well understood. Here, we demonstrate that the Rho-related GTP-binding protein RHOF is activated by KLF4 in esophageal keratinocytes, leading to the induction of NFκB signaling. Moreover, RHOF is required for NFκB activation by KLF4 in esophageal keratinocytes and is also important for esophageal keratinocyte proliferation and migration. Finally, we find that RHOF is upregulated in eosinophilic esophagitis, an important esophageal inflammatory disease in humans. Thus, RHOF activation of NFκB in esophageal keratinocytes provides a potentially important and clinically-relevant mechanism for esophageal inflammation and inflammation-mediated esophageal squamous cell 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.