ArticleScientific reports2016
High glucose enhances progression of cholangiocarcinoma cells via STAT3 activation.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 91 citations in OpenAlex.
- Glucosamine induces apoptosis of cholangiocarcinoma cells by suppressing high-mannose typeFuture science OA · 2026Article
- Association Between Metabolic Syndrome and Long-Term Prognosis in Patients with Perihilar Cholangiocarcinoma Treated with Curative-Intent Resection: A Multicenter Study.Annals of surgical oncology · 2026Article
- iRhom2 deletion protects against diabetic neuropathy by suppressing neuroinflammation.The Journal of pharmacology and experimental therapeutics · 2026Article
- Article
- Modulation of Tumor Metabolism in Acute Leukemia by Plant-Derived Polymolecular Drugs and Their Effects on Mitochondrial Function.Molecules (Basel, Switzerland) · 2025Article
- The role of transketolase in the immunotherapy and prognosis of hepatocellular carcinoma: a multi-omics approach.Frontiers in immunology · 2025Article
- HKDC1 functions as a glucose sensor and promotes metabolic adaptation and cancer growth via interaction with PHB2.Cell death and differentiation · 2024Article
- Liraglutide exhibits potential anti-tumor effects on the progression of intrahepatic cholangiocarcinoma, in vitro and in vivo.Scientific reports · 2024Article
- Melatonin Inhibits AGS Cell Proliferation by Binding to the ATP Binding Site of CDK2 Under Hyperglycemic Conditions.Cell biochemistry and biophysics · 2024Article
- CD161Oncoimmunology · 2024Article
- Involvement of interleukin-1β in high glucose-activated proliferation of cholangiocarcinoma.Translational gastroenterology and hepatology · 2024Article
- Effects of T2DM on cancer progression: pivotal precipitating factors and underlying mechanisms.Frontiers in endocrinology · 2024Review
- γ-aminobutyric acid B2 receptor: A potential therapeutic target for cholangiocarcinoma in patients with diabetes mellitus.World journal of gastroenterology · 2023Article
- Lactic acidosis induces metabolic and phenotypic reprogramming in cholangiocarcinoma cells via the upregulation of thrombospondin-1.Cancer science · 2023Article
- Article
- Glucose Increases STAT3 Activation, Promoting Sustained XRCC1 Expression and Increasing DNA Repair.International journal of molecular sciences · 2022Article
- Metabolic Phenotyping Predicts Gemcitabine and Cisplatin Chemosensitivity in Patients With Cholangiocarcinoma.Frontiers in public health · 2022Article
- Article
- Cholangiocarcinoma.Nature reviews. Disease primers · 2021Review
- High glucose: an emerging association between diabetes mellitus and cancer progression.Journal of molecular medicine (Berlin, Germany) · 2021Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epidemiological studies have indicated diabetes mellitus (DM) as a risk of cholangiocarcinoma (CCA), however, the effects and mechanisms of high glucose on progression of CCA remain unclear. This study reports for the first time of the enhancing effects of high glucose on aggressive phenotypes of CCA cells via STAT3 activation. CCA cells cultured in high glucose media exerted significantly higher rates of cell proliferation, adhesion, migration and invasion than those cultured in normal glucose. The phosphokinase array revealed STAT3 as the dominant signal activated in response to high glucose. Increased nuclear STAT3, p-STAT3 and its downstream target proteins, cyclin D1, vimentin and MMP2, were shown to be underling mechanisms of high glucose stimulation. The link of high glucose and STAT3 activation was confirmed in tumor tissues from CCA patients with DM that exhibited higher STAT3 activation than those without DM. Moreover, the levels of STAT3 activation were correlated with the levels of blood glucose. Finally, decreasing the level of glucose or using a STAT3 inhibitor could reduce the effects of high glucose. These findings suggest that controlling blood glucose or using a STAT3 inhibitor as an alternative approach may improve the therapeutic outcome of CCA patients with DM.
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