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Metformin, cancer and glucose metabolism

Barbara Salani1, Alberto Del Rio1, Cecilia Marini2

  • 1Department of Internal Medicine (DIMI)University of Genova, Viale Benedetto XV/6, 16132 Genova, ItalyIRCCS Azienda Ospedaliera Universitaria San Martino - IST Istituto Nazionale per la Ricerca sul Cancro16132 Genova, ItalyDepartment of ExperimentalDiagnostic and Specialty Medicine (DIMES), Alma Mater Studiorum, University of Bologna, Bologna, ItalyCNR Institute of Organic Synthesis and Photoreactivity (ISOF)40129 Bologna, ItalyCNR Institute of Molecular Bioimaging and Physiology (IBFM)16132 Genova, ItalyDepartment of Health Science (DISSAL)University of Genova, 16132 Genova, Italy Department of Internal Medicine (DIMI)University of Genova, Viale Benedetto XV/6, 16132 Genova, ItalyIRCCS Azienda Ospedaliera Universitaria San Martino - IST Istituto Nazionale per la Ricerca sul Cancro16132 Genova, ItalyDepartment of ExperimentalDiagnostic and Specialty Medicine (DIMES), Alma Mater Studiorum, University of Bologna, Bologna, ItalyCNR Institute of Organic Synthesis and Photoreactivity (ISOF)40129 Bologna, ItalyCNR Institute of Molecular Bioimaging and Physiology (IBFM)16132 Genova, ItalyDepartment of Health Science (DISSAL)University of Genova, 16132 Genova, Italy.

Endocrine-Related Cancer
|October 3, 2014
PubMed

Insights

Metformin, a type 2 diabetes drug, may lower cancer risk by targeting glucose metabolism. It reduces cellular energy and ATP production, impacting cancer cell growth.

Area of Science:

  • Biochemistry
  • Oncology
  • Pharmacology

Background:

  • Metformin is a primary treatment for type 2 diabetes.
  • Clinical studies suggest metformin use correlates with reduced cancer risk in diabetic patients.
  • Malignant transformation involves altered glucose metabolism, specifically increased glycolysis.

Purpose of the Study:

  • To review molecular mechanisms linking metformin's anticancer effects to glucose metabolism.
  • To explore metformin's impact on glycolysis in normal and cancerous cells.
  • To consider metformin's role in drug discovery for cancer treatment.

Main Methods:

  • Review of recent scientific literature on metformin, cancer, and glucose metabolism.
  • Analysis of metformin's effects on cellular energy production (ATP) and AMP-activated protein kinase (AMPK).
  • Investigation into metformin's inhibition of hexokinase-II and its impact on glucose phosphorylation.

Main Results:

  • Metformin decreases mitochondrial respiration and ATP production.
  • Activation of AMP-activated protein kinase (AMPK) by metformin helps regulate energy homeostasis.
  • Metformin inhibits hexokinase-II, reducing glucose uptake and utilization by cancer cells.

Conclusions:

  • Metformin's anticancer properties are linked to its modulation of glucose metabolism.
  • Targeting glycolysis with metformin presents a potential strategy for cancer therapy.
  • Further research into metformin's effects on cancer cells could yield new drug discovery avenues.
Keywords:
AMPKCancerGlucoseHexokinaseMetformin

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