Related Experiment Video
Updated: Jan 13, 2026

Intramucosal Inoculation of Squamous Cell Carcinoma Cells in Mice for Tumor Immune Profiling and Treatment Response Assessment
Published on: April 22, 2019
Biological Anti-Tumoral Mechanisms of Metformin in Head and Neck Squamous Cell Carcinomas: A Systematic Review
Thibaut Buset1, Antoine Yanni1, Margaux Gerbaux2
1Department of Stomatology-Maxillofacial Surgery, CHU-Saint-Pierre, Université Libre de Bruxelles (ULB), 1000 Brussels, Belgium.
Abstract:
Background/Objectives: Recent studies suggest Metformin could be a potential anti-tumoral agent. This review aims to understand the biological anti-tumoral mechanisms of Metformin in head and neck cancer squamous cell carcinomas (HNSCC) both in vitro and in vivo. Methods: Two investigators screened publications on the biological anti-tumoral effects of Metformin in HNSCC. The literature search was conducted on PubMed, Cochrane Library, and Scopus using PICOTS and PRISMA statements. Results: A total of 30 papers were identified, including 18 studies exploring the effect of Metformin alone and 12 studies exploring its effect in association with another drug or therapy for HNSCC lines. The results suggest that Metformin decreases the proliferation rate of HNSCC through inhibition of cell proliferation by the induction of G0/G1 cell cycle arrest and activation of apoptosis, by regulating proteins involved in carcinogenesis pathways, and also affects the tumor microenvironment by switching the metabolism and activating immune cells. In addition, Metformin can potentiate the efficiency and/or sensibility of other anti-tumoral treatments. The present systematic review highlights the biological anti-tumoral effects of Metformin used alone or in combination with traditional therapies for HNSCC. Conclusions: This review of the literature summarizes the biological anti-tumoral effects associated with Metformin alone or in combination with other therapies. While the molecular effects of Metformin on signaling pathways are different when used alone than in combination, they converge in a decreased proliferation of tumor cells and/or a sensitization of HNSCC to other anti-cancer therapies.
Insights
Metformin demonstrates anti-tumoral effects in head and neck squamous cell carcinomas (HNSCC) by inhibiting cell proliferation and inducing apoptosis. It also enhances other cancer therapies, offering a potential therapeutic strategy for HNSCC.
Area of Science:
- Oncology
- Pharmacology
- Cancer Biology
Background:
- Emerging research indicates Metformin possesses potential anti-tumoral properties.
- Head and neck cancer squamous cell carcinomas (HNSCC) are a significant area of oncological research.
- Understanding Metformin's mechanisms in HNSCC is crucial for developing new therapeutic strategies.
Purpose of the Study:
- To systematically review the biological anti-tumoral mechanisms of Metformin in HNSCC.
- To analyze Metformin's effects both in vitro and in vivo.
- To evaluate Metformin's efficacy as a standalone agent and in combination therapies.
Main Methods:
- A comprehensive literature search was performed on PubMed, Cochrane Library, and Scopus.
- Publications were screened by two independent investigators using PICOTS and PRISMA guidelines.
- A total of 30 relevant studies were identified and analyzed.
Main Results:
- Metformin significantly decreases HNSCC proliferation by inducing G0/G1 cell cycle arrest and apoptosis.
- It regulates key proteins in carcinogenesis pathways and modulates the tumor microenvironment.
- Metformin enhances the efficacy and sensitivity of other anti-tumoral treatments for HNSCC.
Conclusions:
- Metformin exhibits significant biological anti-tumoral effects in HNSCC, both alone and in combination therapies.
- Molecular mechanisms differ when Metformin is used alone versus in combination.
- These effects converge to reduce tumor cell proliferation and sensitize HNSCC to anti-cancer therapies.
Related Concept Videos
Oral Hypoglycemic Agents: Biguanides and Glitazones
Cancer Therapies
However, cancer treatments can pose several challenges, as therapies used to kill cancer cells are generally also toxic to normal cells. Moreover, cancer cells mutate rapidly and can develop resistance to chemical agents or radiation therapy. Besides, all types of cancer cells may not respond to the same therapy. Some cancer cells respond to one...

