ArticleActa pharmacologica Sinica2019
Aspirin inhibits the proliferation of hepatoma cells through controlling GLUT1-mediated glucose metabolism.
Article in Acta pharmacologica Sinica, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.
What it found
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Who cites it
35 citing papers in PubMed, 1 synthesis or guideline pooled it, 66 citations in OpenAlex.
- The relationship between aspirin consumption and hepatocellular carcinoma: a systematic review and meta-analysis.European journal of medical research · 2023Pooled it
- Aspirin reduces short-term mortality risk in critically ill patients with liver cirrhosis: a propensity-score matched retrospective analysis using the MIMIC-IV database.BMC gastroenterology · 2025Article
- Metabolic reprogramming in hepatocellular carcinoma: mechanisms of immune evasion and therapeutic implications.Frontiers in immunology · 2025Review
- Aspirin in Cancer Therapy: Pharmacology and Nanotechnology Advances.International journal of nanomedicine · 2025Review
- Drug Repurposing: A Conduit to Unravelling Metabolic Reprogramming for Cancer Treatment.Mini reviews in medicinal chemistry · 2025Review
- Article
- The role of metabolic reprogramming in liver cancer and its clinical perspectives.Frontiers in oncology · 2024Review
- Effect of Low-Dose Aspirin Use After Thermal Ablation in Patients with Hepatocellular Carcinoma: A Retrospective Study.Journal of hepatocellular carcinoma · 2024Article
- Nanomicelles for GLUT1-targeting hepatocellular carcinoma therapy based on NADPH depletion.Drug delivery · 2023Article
- Aspirin reprogrammes colorectal cancer cell metabolism and sensitises to glutaminase inhibition.Cancer & metabolism · 2023Article
- Aspirin triggers ferroptosis in hepatocellular carcinoma cells through restricting NF-κB p65-activated SLC7A11 transcription.Acta pharmacologica Sinica · 2023Article
- Improving Management of Portal Hypertension: The Potential Benefit of Non-Etiological Therapies in Cirrhosis.Journal of clinical medicine · 2023Review
- Aspirin and the metabolic hallmark of cancer: novel therapeutic opportunities for colorectal cancer.Exploration of targeted anti-tumor therapy · 2023Review
- The role of antiplatelet therapies on incidence and mortality of hepatocellular carcinoma.European journal of clinical investigation · 2023Article
- Innovative targets of the lncRNA-miR-mRNA network in response to low-dose aspirin in breast cancer patients.Scientific reports · 2022Article
- Review
- Modulation of Reactive Oxygen Species Homeostasis as a Pleiotropic Effect of Commonly Used Drugs.Frontiers in aging · 2022Review
- Targeting the Interplay between Cancer Metabolic Reprogramming and Cell Death Pathways as a Viable Therapeutic Path.Biomedicines · 2021Review
- lncRNA GAS6-AS1 inhibits progression and glucose metabolism reprogramming in LUAD via repressing E2F1-mediated transcription of GLUT1.Molecular therapy. Nucleic acids · 2021Article
- Aspirin inhibits cholangiocarcinoma cell proliferation via cell cycle arrest in vitro and in vivo.International journal of oncology · 2021Article
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aspirin can efficiently inhibit liver cancer growth, but the mechanism is poorly understood. In this study, we report that aspirin modulates glucose uptake through downregulating glucose transporter 1 (GLUT1), leading to the inhibition of hepatoma cell proliferation. Our data showed that aspirin significantly decreased the levels of reactive oxygen species (ROS) and glucose consumption in hepatoma cells. Interestingly, we identified that GLUT1 and HIF1α could be decreased by aspirin. Mechanically, we demonstrated that the -1008/-780 region was the regulatory element of transcriptional factor NF-κB in GLUT1 promoter by luciferase report gene assays. PDTC, an inhibitor of NF-κB, could suppress the expression of GLUT1 in HepG2 and H7402 cells, followed by affecting the levels of ROS and glucose consumption. CoCl
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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.