Abstract
Cancer cells display enhanced growth rates and a resistance to apoptosis. The ability of cancer cells to evade homeostasis and proliferate uncontrollably while avoiding programmed cell death/apoptosis is acquired through mutations to key signaling molecules, which regulate pathways involved in cell proliferation and survival and these mutations allow them to develop resistance to many chemotherapeutic agents, highlighting the need for development of new potent anti-cancer agents. Metformin has long been used as a treatment for type 2 diabetes and has recently attracted attention as a potential agent to be used in the treatment of cancer. The present review summarizes the existing in vitro and in vivo animal studies focusing on the anti-lung cancer effects of metformin and its effects on key proliferative and anti-apoptotic signaling pathways.
Highlights
Cancer cells are characterized by their high rate of proliferation and resistance to apoptotic cell death [1]
Growth factors bind to their receptors, receptor auto-phosphorylation occurs leading to activation of downstream signaling cascades such as the phosphoinositide-3-kinase (PI3K)/Protein kinase B (Akt)/mammalian target of rapamycin pathway that results in increased survival/proliferation and inhibition of apoptosis [10,11,12,13]
Sayed et al [87] conducted a randomized controlled study on stage IV non-small-cell lung cancer (NSCLC) non diabetic patients receiving gemcitabine/cisplatin alone or in combination with metformin (500 mg daily) and found that in the combination group compared to the gemcitabine/cisplatin treatment alone, the objective response rate was 46.7% compared to 13.3% (p = 0.109), the overall survival was 12 months compared to 6.5 months (p = 0.119) and the median progression free survival was
Summary
Cancer cells are characterized by their high rate of proliferation and resistance to apoptotic cell death [1]. Growth factors bind to their receptors, receptor auto-phosphorylation occurs leading to activation of downstream signaling cascades such as the phosphoinositide-3-kinase (PI3K)/Protein kinase B (Akt)/mammalian target of rapamycin (mTOR) pathway that results in increased survival/proliferation and inhibition of apoptosis [10,11,12,13]. We summarize all in vitro and in vivo animal studies examining the effects of metformin in lung cancer. The studies presented in the text are summarized, organized and presented in a table format to allow the reader to extract the information This is a comprehensive systematic review and adds to the existing literature by summarizing all relevant in vitro and in vivo animal studies using metformin in lung cancer
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