Diabetes Drug Metformin Shows Early Promise Against Skin Cancer in New Review
A review of 20 studies suggests metformin may help prevent and treat skin cancers, with the strongest signal in basal cell carcinoma. Trials are still needed.
Summary
Metformin, a decades-old diabetes drug, is drawing attention for possible anticancer effects. This structured review examined 20 studies on how it affects melanoma, basal cell carcinoma (BCC), and squamous cell carcinoma (SCC). In melanoma models, metformin slowed tumor growth, curbed cell changes linked to spread, and boosted immune responses. Human observational data suggested better recurrence-free survival in some melanoma patients, though results were inconsistent. For nonmelanoma skin cancers, metformin use was linked to fewer BCC and SCC cases, and lab studies showed delayed tumor development and improved response to photodynamic therapy. The authors judge the evidence strongest for BCC. Metformin appears biologically plausible as a low-cost, well-tolerated add-on therapy, but prospective controlled trials are still needed to confirm benefit, set dosing, and identify who gains most.
Detailed Summary
Skin cancers are the most common malignancies worldwide, and melanoma remains dangerous once it spreads. Metformin is cheap, widely available, and has a long safety record in type 2 diabetes. Its effects on metabolic and immune pathways have made it a candidate for repurposing in oncology, including dermatology.
The authors ran a structured PubMed search in April 2025 for English-language original research on metformin in melanoma, BCC, and SCC. They included experimental, observational, and clinical studies and excluded reviews and meta-analyses. Twenty studies met the criteria.
In melanoma models, metformin inhibited tumor proliferation, suppressed epithelial-mesenchymal transition (a process tied to invasion and metastasis), and enhanced immune responses. Observational human studies reported improved recurrence-free survival and treatment outcomes in some cases, but findings were inconsistent. In nonmelanoma skin cancer, metformin use was associated with lower incidence of BCC and SCC. Preclinical work showed delayed tumor development and a better response to photodynamic therapy after metformin treatment.
The authors conclude that the evidence is strongest for BCC, particularly for enhancing photodynamic therapy and reducing incidence in at-risk groups. In melanoma, metformin may work synergistically with immunotherapy, but clinical results vary. Overall, they describe it as a promising, low-cost, well-tolerated adjunct in dermatologic oncology.
Several caveats apply. Much of the support comes from preclinical models and observational data, which cannot prove causation and can be confounded by diabetes status and other factors. Only the abstract was available, so study-level details, effect sizes, and doses are unknown. The authors call for prospective, controlled studies to clarify efficacy, optimize dosing, and identify the populations most likely to benefit.
Key Findings
- Twenty studies met inclusion criteria, spanning experimental, observational, and clinical research on melanoma, BCC, and SCC.
- In melanoma models, metformin inhibited proliferation, suppressed epithelial-mesenchymal transition, and enhanced immune responses.
- Observational melanoma studies reported improved recurrence-free survival and outcomes, but findings were inconsistent across studies.
- Metformin use was associated with reduced incidence of both BCC and SCC in nonmelanoma skin cancer studies.
- Preclinical models showed delayed tumor development and enhanced photodynamic therapy response; the authors rate evidence strongest for BCC.
Methodology
This is a structured literature review based on a April 2025 PubMed search for English-language, peer-reviewed original studies of metformin in melanoma, BCC, and SCC. Experimental, observational, and clinical studies were included, while reviews and meta-analyses were excluded, yielding 20 studies. The abstract does not describe formal quality assessment or quantitative pooling.
Study Limitations
Much of the evidence is preclinical or observational, which limits causal inference and may reflect confounding by diabetes status or other factors. Melanoma findings were inconsistent, and optimal dosing and responsive populations remain undefined. This summary is based on the abstract only, so study-level data, effect sizes, and risk of bias could not be evaluated.
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