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.

PubMed

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.