Cited by 37Metabolism, Diabetes, and CancerCancer, Hypoxia, and MetabolismPI3K/AKT/mTOR signaling in cancer

Metformin and cancer: licence to heal?

Papanas, Nikolaos, Maltezos, Efstratios, Mikhailidis, Dimitri P·2010·Expert Opinion on Investigational Drugs

Abstract

Type 2 diabetes mellitus is associated with increased risk of malignancy (mainly cancer of the pancreas, breast, colon, endometrium and bladder). In addition, there is evidence that antidiabetic medication may itself affect the risk of cancer. Importantly, metformin is nowadays emerging as an agent that has the potential to protect from cancer. Population studies have shown that metformin is associated with a significant reduction of neoplasias in general (and cancer of the breast and prostate, in particular). These observations are supported by in vitro and in vivo evidence that metformin inhibits the growth of cancer cells. The mechanisms underlying this protective potential of metformin are not completely understood. While other mechanisms have also been proposed, the protective action of metformin appears to be exerted by two main pathways. The first involves reduction of endogenous hyperinsulinemia. The second pathway relates to the activation of adenosine monophosphate-activated protein kinase (AMPK), which is recognized to inhibit cellular protein synthesis and growth. Whatever the precise mechanism, any reduction in the risk for cancer may be far-reaching, and this favorable effect adds to the clinical value of metformin as the mainstay of antidiabetic treatment.

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Crossref · 10.1517/13543784.2010.499122

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  • Patients with type 2 diabetes have increased risks of various types of cancer, particularly liver, pancreas, endometrium, colon, rectum, breast, and bladder cancer.

    “Patients with type 2 diabetes have increased risks of various types of cancer, particularly liver, pancreas, endometrium, colon, rectum, breast, and bladder cancer.”
  • Metformin's anticancer effect may be due to effects on insulin reduction and hyperinsulinemia, and consequently on IGF-1 levels, but may also involve specific AMPK-mediated pathways.

    “It may be due to its effects on insulin reduction and hyperinsulinemia, and consequently on IGF-1 levels, which have mitogenic actions enhancing cellular proliferation,but may also involve specific AMPK-mediated pathways [133].”
  • Metformin significantly reduces tumorigenesis and cancer cell growth.

    “Metformin significantly reduces tumorigenesis and cancer cell growth although how it does it is not well understood.”
  • Cancer mortality is increased in patients with type 2 diabetes.

    “Cancer mortality is also increased [133,134].”

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References 45 · Cited by 37

Authors
Papanas, N., Maltezos, E., & Mikhailidis, D. P.
Affiliations
  • Democritus University of Thrace (GR)
  • The Royal Free Hospital (GB)
Venue
Expert Opinion on Investigational Drugs
Published
2010-06-18
Volume
19
Issue
8
Pages
913-917
ISSN
  • 1354-3784 (ISSN-L)
  • 1744-7658
OpenAlex
W2047844250
Cited by
37
References
45
Citations by year
2024: 1 · 2023: 4 · 2022: 1 · 2021: 3 · 2020: 1 · 2018: 2 · 2017: 4 · 2016: 1 · 2015: 3 · 2014: 1 · 2013: 3 · 2012: 6
FWCI
2.08
Type
journal article
Language
en
Open access
closed
Locations
  • Expert Opinion on Investigational Drugs (publishedVersion)
  • PubMed (publishedVersion)
  • UCL Discovery (University College London) (submittedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
Keywords
metformin, cancer risk, type 2 diabetes, hyperinsulinemia, AMPK, breast cancer, prostate cancer, chemoprevention, antidiabetic drugs, pancreatic cancer, colon cancer, endometrial cancer, bladder cancer
MeSH terms
AMP-Activated Protein Kinase Kinases, Animals, Diabetes Mellitus, Type 2, Female, Humans, Hyperinsulinism, Hypoglycemic Agents, Metformin, Mice, Transgenic, Neoplasms, Protein Kinases, Cell Line, Tumor, Mice

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