ArticleScientific reports2017
Metformin transiently inhibits colorectal cancer cell proliferation as a result of either AMPK activation or increased ROS production.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers, 1 of them a synthesis that pooled it.
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Who cites it
76 citing papers in PubMed, 1 synthesis or guideline pooled it, 130 citations in OpenAlex.
- AMPK variant, a candidate of novel predictor for chemotherapy in metastatic colorectal cancer: A meta-analysis using TRIBE, MAVERICC and FIRE3.International journal of cancer · 2019Pooled it
- Comparison of Metformin Combinations with Other Repurposed Drugs in the Treatment of Hamster Fibrosarcoma: A Review.Pharmaceuticals (Basel, Switzerland) · 2026Review
- p53 and p21 Status Influences Cellular Response to Metformin inCurrent issues in molecular biology · 2026Article
- Dose-Response Relationship of Niclosamide and Metformin Combination in ApcGut and liver · 2026Article
- Metformin in gastrointestinal cancers and inflammatory bowel disease: Unraveling its mechanisms and therapeutic applications.iScience · 2026Review
- Review
- Design, synthesis, biological evaluation and molecular docking of novel isatin-oxime ether derivatives as potential IDH1 inhibitors.Molecular diversity · 2025Article
- Additive Anticancer and Antioxidant Effects of Metformin and Luteolin in Breast and Colorectal Cancer Cell Lines.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Nanocomposite biosensor tracks honokiol-induced oxidative stress dynamics in 3D hydrogel-cultured lung cancer cells.Microsystems & nanoengineering · 2025Article
- Metformin in Colorectal Cancer: Epidemiological Evidence, Predictive Biomarkers, and Implications for Prevention and Treatment.International journal of molecular sciences · 2025Review
- Chemoprevention of Colorectal Cancer-With Emphasis on Low-Dose Aspirin and Anticoagulants.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Modulation of the Antitumor Response to Metformin, Caffeine, and Sodium Dichloroacetate by the Hypoxic Microenvironment in Lung Cancer Cells.International journal of molecular sciences · 2025Article
- The crosstalk between non-coding RNAs and oxidative stress in cancer progression.Genes & diseases · 2025Review
- Metformin modulates FJX1 via upregulation of Hsa-miR-1306-3p to suppress colon adenocarcinoma viability.Scientific reports · 2025Article
- Effect of metformin on cell proliferation and apoptosis in steatosis HepG2 cell model.Northern clinics of Istanbul · 2025Article
- Design, Synthesis, Anti-Proliferative Effects, and Mechanistic Details of Fluorine-Containing Biguanide Derivatives with Various Carbon Rings.Medicinal chemistry (Shariqah (United Arab Emirates)) · 2025Article
- Reversal of metformin's anti-proliferative effect in fission yeastnpj metabolic health and disease · 2025Article
- Metformin Against Herpes Zoster in Colon Cancer Patients with Type 2 Diabetes: A PSM Analysis.Journal of Cancer · 2025Article
- Non-coding RNAs as potential targets in metformin therapy for cancer.Cancer cell international · 2024Review
- Metformin's role in lowering colorectal cancer risk among individuals with diabetes from the Southern Community Cohort Study.Cancer epidemiology · 2024Article
16 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Metformin is a widely used and well-tolerated anti-diabetic drug that can reduce cancer risk and improve the prognosis of certain malignancies. However, the mechanism underlying its anti-cancer effect is still unclear. We studied the anti-cancer activity of metformin on colorectal cancer (CRC) by using the drug to treat HT29, HCT116 and HCT116 p53-/- CRC cells. Metformin reduced cell proliferation and migration by inducing cell cycle arrest in the G0/G1 phase. This was accompanied by a sharp decrease in the expression of c-Myc and down-regulation of IGF1R. The anti-proliferative action of metformin was mediated by two different mechanisms: AMPK activation and increase in the production of reactive oxygen species, which suppressed the mTOR pathway and its downstream targets S6 and 4EBP1. A reduction in CD44 and LGR5 expression suggested that the drug had an effect on tumour cells with stem characteristics. However, a colony formation assay showed that metformin slowed the cells' ability to form colonies without arresting cell growth, as confirmed by absence of apoptosis, autophagy or senescence. Our finding that metformin only transiently arrests CRC cell growth suggests that efforts should be made to identify compounds that combined with the biguanide can act synergistically to induce cell death.
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