ArticleLife sciences2020
NF-κB and STAT3 co-operation enhances high glucose induced aggressiveness of cholangiocarcinoma cells.
Article in Life sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 25 citations in OpenAlex.
- Glucosamine induces apoptosis of cholangiocarcinoma cells by suppressing high-mannose typeFuture science OA · 2026Article
- Impact of dynamic blood glucose trajectories on mortality in critically ill non-traumatic intracranial hemorrhage patients: a retrospective cohort study.BMC neurology · 2026Article
- Influence of Extraction Method on the Bioactivity ofFoods (Basel, Switzerland) · 2026Article
- Unveiling the role of stress hyperglycemia in predicting mortality for critically ill hemorrhagic stroke patients: insights from MIMIC-IV.Frontiers in endocrinology · 2025Article
- The Clinical Application of GLP-1RAs and GLP-1/GIP Dual Receptor Agonists Based on Pharmacological Mechanisms: A Review.Drug design, development and therapy · 2025Review
- Review
- Glucagon-like peptide 1 receptor agonist: A potential game changer for cholangiocarcinoma.World journal of gastroenterology · 2024Article
- Liraglutide exhibits potential anti-tumor effects on the progression of intrahepatic cholangiocarcinoma, in vitro and in vivo.Scientific reports · 2024Article
- Immunometabolic alterations in type 2 diabetes mellitus revealed by single-cell RNA sequencing: insights into subtypes and therapeutic targets.Frontiers in immunology · 2024Article
- Involvement of interleukin-1β in high glucose-activated proliferation of cholangiocarcinoma.Translational gastroenterology and hepatology · 2024Article
- Cornuside inhibits glucose-induced proliferation and inflammatory response of mesangial cells.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2023Article
- γ-aminobutyric acid B2 receptor: A potential therapeutic target for cholangiocarcinoma in patients with diabetes mellitus.World journal of gastroenterology · 2023Article
- Article
- Glucose Increases STAT3 Activation, Promoting Sustained XRCC1 Expression and Increasing DNA Repair.International journal of molecular sciences · 2022Article
- Hyperglycemia AltersIn vivo (Athens, Greece)Article
- Behavioral Medicine in Cholangiocarcinoma: Bridging the Gap Between Biology and Behavior.Cancer control : journal of the Moffitt Cancer CenterReview
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 3 countries.
Funding
Abstract
aimsThe present report aimed to investigate the underlying genes and pathways of high glucose driving cholangiocarcinoma (CCA) aggressiveness. MAIN
methodsWe screened and compared the gene expression profiles obtained by RNA sequencing, of CCA cells cultured in high and normal glucose. Results from the transcriptomic analysis were confirmed in additional cell lines using in vitro migration-invasion assay, Western blotting and immunocytofluorescence. KEY
findingsData indicated that high glucose increased the expression of interleukin-1β (IL-1β), an upstream regulator of nuclear factor-κB (NF-κB) pathway, through the nuclear localization of NF-κB. High glucose-induced NF-κB increased the migration and invasion of CCA cells and the expression of downstream NF-κB targeted genes associated with aggressiveness, including interleukin-6, a potent triggering signal of the signal transducer and activator of transcription 3 (STAT3) pathway. Such effects were reversed by inhibiting NF-κB nuclear translocation which additionally reduced the phosphorylation of STAT3 at Y705. SIGNIFICANCE: These results indicate that NF-κB is activated by high glucose and they suggest that NF-κB interaction with STAT3 enhances CCA aggressiveness. Therefore, targeting multiple pathways such as STAT3 and NF-κB might improve CCA treatment outcome especially in condition such as hyperglycemia.
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