ArticleCell death & disease2019
Canagliflozin inhibits growth of hepatocellular carcinoma via blocking glucose-influx-induced β-catenin activation.
Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 2 of them syntheses that pooled it.
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Who cites it
53 citing papers in PubMed, 2 syntheses or guidelines pooled it, 90 citations in OpenAlex.
- The correlation between novel antidiabetic agents utilization and hepatocellular carcinoma incidence in type 2 diabetes patients: a network meta-analysis.European journal of clinical pharmacology · 2025Pooled it
- Efficacy of SGLT2 inhibitors for anthracycline-induced cardiotoxicity: a meta-analysis in cancer patients.Future cardiology · 2024Pooled it
- Article
- Serum uric acid and its metabolism-a vital factor in the inflammatory transformation of cancer.Journal of advanced research · 2026Review
- SGLT2 inhibitor use reduces progression and surgical intervention of persistent pulmonary nodules.Lung cancer (Amsterdam, Netherlands) · 2026Article
- Metabolic Concepts of Sodium-Glucose Cotransporter 2 Inhibitors-Based Therapies Against Hepatocarcinogenesis and Therapy Resistance in Hepatocellular Carcinoma.Life (Basel, Switzerland) · 2026Review
- Insulin resistance: mechanisms and therapeutic interventions.Molecular biomedicine · 2026Review
- Synthetic Flozins in Cancer Prevention and Combination Strategies: Structural Insights and Therapeutic Potential.Molecules (Basel, Switzerland) · 2025Review
- Canagliflozin synergises with serine restriction mediating anti-leukaemic effects in T-cell acute lymphoblastic leukaemia.Molecular metabolism · 2025Article
- Anti-diabetic medications and cancer: links beyond glycemic and body weight control.Precision clinical medicine · 2025Review
- Therapeutic efficacy of canagliflozin against hepatocarcinogenesis induced by CDD/DEN/TAA in a rat model: regulation of AMPK/HIF-1α/YAP-1/TAZ signaling pathways.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Potential anticancer effects of sodium-glucose cotransporter protein 2 (SGLT2) inhibitors Canagliflozin and Dapagliflozin.Cancer chemotherapy and pharmacology · 2025Review
- Unveiling the anticancer potential of SGLT-2 inhibitors: mechanisms and prospects in clinical oncology-a narrative review.European journal of medical research · 2025Review
- Review
- Article
- Exploring the Role of SGLT2 Inhibitors in Cancer: Mechanisms of Action and Therapeutic Opportunities.Cancers · 2025Review
- Advances in sodium-glucose transporter protein 2 inhibitors and tumors.Frontiers in oncology · 2025Review
- Research Progress of SGLT2 Inhibitors in Cancer Treatment.Drug design, development and therapy · 2025Review
- Anti-Diabetic Therapies and Cancer: From Bench to Bedside.Biomolecules · 2024Review
- Canagliflozin alleviates pulmonary hypertension by activating PPARγ and inhibiting its S225 phosphorylation.Acta pharmacologica Sinica · 2024Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Accelerated glucose metabolism is critical in hepatocarcinogenesis, but the utilities of different glucose transporter inhibitors in treating hepatocellular carcinoma (HCC) remain largely uncharacterized. In this study, we examined a collection of glucose transporter inhibitors and found differential anti-HCC effects among these compounds. Canagliflozin (CANA), phloretin, and WZB117 decreased cellular glucose influx, but only CANA showed potent growth inhibition in HCC, which indicated a glucose-independent anti-HCC mechanism. Notably, we found that CANA treatment significantly downregulated the expression of β-catenin in HCC cells in. By co-treating cells with cycloheximide and MG-132, we proved that CANA promoted proteasomal degradation of β-catenin protein by increasing phosphorylation of β-catenin, and CANA-induced inactivation of protein phosphatase 2A was identified being responsible for this effect. Moreover, using Huh7 xenografted tumor model, CANA treatment was shown to delay tumor growth and improved the survival of HCC bearing mice. Our study highlights the unique dual β-catenin-inhibition mechanisms of CANA, which may provide new thoughts on treating HCC patient with concurrent diabetes, and, furthermore, on developing novel treatment targeting metabolic reprogram and/or WNT/β-catenin signaling in HCC.
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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.