ArticleExperimental and therapeutic medicine2021
Diclofenac impairs the proliferation and glucose metabolism of triple-negative breast cancer cells by targeting the c-Myc pathway.
Article in Experimental and therapeutic medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 35 citations in OpenAlex.
- Comparison of Metformin Combinations with Other Repurposed Drugs in the Treatment of Hamster Fibrosarcoma: A Review.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Olaparib alleviates diclofenac-induced toxicity in HepG2 cells via modulation of oxidative stress and mitochondrial functions.Molecular and cellular biochemistry · 2026Article
- Oncogene c‑Myc: From molecular mechanism to targeted therapy (Review).Molecular medicine reports · 2026Review
- Repurposing diclofenac for combination therapy: targeting the Warburg effect to enhance breast cancer treatment.Turkish journal of medical sciences · 2026Article
- Glucose metabolic reprogramming: a novel strategy to enhance radiotherapy response to triple-negative breast cancer.Frontiers in public health · 2026Review
- Rutin-encapsulated manganese carbonate nanoparticles for 'liver-dark/tumor-bright' magnetic resonance imaging and inhibition of breast cancer with liver metastases.Regenerative biomaterials · 2026Article
- The Road to Precision Nanomedicine: An Insight on Drug Repurposing and Advances in Nanoformulations for Treatment of Cancer.AAPS PharmSciTech · 2025Review
- Bioinformatics Strategies in Breast Cancer Research.Biomolecules · 2025Review
- Synergistic Effects of 2-Deoxyglucose and Diclofenac Sodium on Breast Cancer Cells: A Comparative Evaluation of MDA-231 and MCF7 Cells.International journal of molecular sciences · 2025Article
- Energy metabolism in health and diseases.Signal transduction and targeted therapy · 2025Review
- Drug Repurposing: A Conduit to Unravelling Metabolic Reprogramming for Cancer Treatment.Mini reviews in medicinal chemistry · 2025Review
- Article
- Contribution of non-steroidal anti-inflammatory drugs to breast cancer treatment:Veterinary world · 2024Review
- The Molecular Mechanisms behind Advanced Breast Cancer Metabolism: Warburg Effect, OXPHOS, and Calcium.Frontiers in bioscience (Landmark edition) · 2024Review
- Role of Harmaline in Inhibiting c-Myc, Altering Molecular Typing, and Promoting Apoptosis in Triple-Negative Breast Cancer.Breast cancer (Dove Medical Press) · 2024Article
- miR-22-enriched breast cancer cells display repressed glycolytic metabolism, increased glycogen synthesis, and reduced survival in low glucose conditions.Molecular biology reports · 2023Article
- Review
- Identification of a 5-gene-risk score model for predicting luminal A-invasive lobular breast cancer survival.Genetica · 2022Article
- Facts and Perspectives: Implications of tumor glycolysis on immunotherapy response in triple negative breast cancer.Frontiers in oncology · 2022Review
- Role of HIF-1α/ERRα in Enhancing Cancer Cell Metabolism and Promoting Resistance of Endometrial Cancer Cells to Pyroptosis.Frontiers in oncology · 2022Review
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Triple-negative breast cancer (TNBC) cells obtain energy mainly through aerobic glycolysis, and their glycolytic rate is significantly higher compared with that of non-TNBC cells. Glucose transporter 1 (GLUT1) is a transmembrane transporter necessary for the entry of glucose into tumor cells, hexokinase (HK) is a key enzyme in the glycolytic pathway, and both are targets of the transcription factor c-Myc. c-Myc can promote aerobic glycolysis by upregulating GLUT1 expression and enhancing HK activity. c-Myc and GLUT1 are highly expressed in TNBC. The non-steroidal anti-inflammatory drug diclofenac can inhibit glycolysis in melanoma cells and thereby promote apoptosis by downregulating c-Myc and GLUT1. To explore the effect of diclofenac on the energy metabolism of TNBC cells and determine the underlying mechanism, a comparative study in two TNBC cell lines (MDA-MB-231 and HCC1937) and one non-TNBC cell line (MCF-7) was conducted. Cell proliferation was detected by Cell Counting Kit-8 (CCK-8) and flow cytometric assays; GLUT1 and c-Myc expression was measured by western blotting. Diclofenac significantly inhibited cell proliferation, downregulated GLUT1 and c-Myc expression, and decreased HK activity in TNBC cells compared with non-TNBC cells. In conclusion, the studies suggested that diclofenac inhibited cell glycolysis and suppressed TNBC cell growth by decreasing GLUT1 protein expression and HK activity through the c-Myc pathway.
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