Metformin is a standard clinical drug used to treat type 2 diabetes mellitus 
(T2DM) and polycystic ovary syndrome. Recently, epidemiological studies and 
meta-analyses have revealed that patients with T2DM have a lower incidence of 
tumor development than healthy controls and that patients diagnosed with cancer 
have a lower risk of mortality when treated with metformin, demonstrating an 
association between metformin and tumorigenesis. In vivo and in vitro studies 
have revealed that metformin has a direct antitumor effect, which may depress 
tumor proliferation and induce the apoptosis, autophagy and cell cycle arrest of 
tumor cells. The mechanism underpinning the antitumor effect of metformin has 
not been well established. Studies have demonstrated that reducing insulin and 
insulin-like growth factor levels in the peripheral blood circulation may lead 
to the inhibition of phosphoinositide 3-kinase/Akt/mechanistic target of 
rapamycin (mTOR) signaling or activation of AMP-activated protein kinase, which 
inhibits mTOR signaling, a process that may be associated with the antitumor 
effect of metformin. The present review primarily focuses on the recent progress 
in understanding the function of metformin in tumor development.