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HERO ID
2756061
Reference Type
Journal Article
Subtype
Review
Title
Diabetes, cancer, and metformin: connections of metabolism and cell proliferation
Author(s)
Gallagher, EJ; Leroith, D
Year
2011
Is Peer Reviewed?
Yes
Journal
Annals of the New York Academy of Sciences
ISSN:
0077-8923
EISSN:
1749-6632
Volume
1243
Page Numbers
54-68
Language
English
PMID
22211893
DOI
10.1111/j.1749-6632.2011.06285.x
Abstract
Diabetes is associated with an increased risk of developing and dying from cancer. This increased risk may be due to hyperglycemia, hyperinsulinemia, and insulin resistance or other factors. Metformin has recently gained much attention as it appears to reduce cancer incidence and improve prognosis of patients with diabetes. In vitro data and animal studies support these findings from human epidemiological studies. Metformin has multiple potential mechanisms by which it inhibits cancer development and growth. For example, metaformin inhibits hepatic gluconeogenesis, thus decreasing circulating glucose levels, and it increases insulin sensitivity, thus reducing circulating insulin levels. Intracellularly, metformin activates AMPK, which decreases protein synthesis and cell proliferation. Metaformin also reduces aromatase activity in the stromal cells of the mammary gland. Finally, metformin may diminish the recurrence and aggressiveness of tumors by reducing the stem cell population and inhibiting epithelial to mesenchymal transition. Here, we discuss the metabolic abnormalities that occur in tumor development and some of the mechanisms through which metformin may alter these pathways and reduce tumor growth.
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