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Review
. 2020 Dec;8(24):1711.
doi: 10.21037/atm-20-1060.

"V体育安卓版" Metformin and ovarian cancer: the evidence

Elina Urpilainen  1 , Ulla Puistola  1 , Stergios Boussios  2   3 , Peeter Karihtala  4   5
Affiliations
Review

Metformin and ovarian cancer: the evidence (V体育ios版)

Elina Urpilainen (V体育官网入口) et al. Ann Transl Med. 2020 Dec.

Abstract

In recent decades, great interest in the off-label use of metformin has arisen as a result of its broad effects on different signaling pathways, with only a few side effects, and low cost. Metformin has been shown to have multiple, dose-dependent preclinical anticancer effects, which can be roughly divided into either direct effects via inhibition of mitochondrial respiratory chain complex I, or indirect effects through lowered glucose, insulin and insulin-like growth factor levels. Further details on in vitro and in vivo anticancer effects specifically in ovarian cancer are continuously reported. Preclinically metformin has clear chemosensitizing effects in ovarian cancer and it is an effective negative regulator of angiogenesis. There are also some epidemiological studies on metformin use in ovarian cancer, but the results of these studies are not as promising as those preclinical studies would indicate. Most preclinical studies have involved metformin concentrations that are many times higher than the pharmacological doses used in patients, which might confound the clinical use of metformin as regards the above-mentioned aspects. In this review we evaluate preclinical and clinical evidence concerning metformin in ovarian cancer treatment. VSports手机版.

Keywords: Diabetes; epidemiology; incidence; survival. V体育安卓版.

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Conflict of interest statement (VSports app下载)

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at http://dx. doi. org/10. 21037/atm-20-1060). The series “Ovarian Cancer: State of the Art and Perspectives of Clinical Research” was commissioned by the editorial office without any funding or sponsorship. SB serves as an unpaid editorial board member of Annals of Translational Medicine from Nov 2019 to Oct 2021 VSports最新版本. EU reports grants from The Cancer Society of Finland, during the conduct of the study. UP reports grants from Jane and Aatos Erkko Foundation, during the conduct of the study. The other authors have no conflicts of interest to declare.

"VSports注册入口" Figures

Figure 1
Figure 1
Metformin affects cancer cells both directly and indirectly. It activates AMP-activated protein kinase (AMPK), which leads, among other things, to inhibition of mammalian target of rapamycin (mTOR). It also sensitizes tissues to insulin, reduces hepatic gluconeogenesis and decreases circulating insulin levels. This leads indirectly to reduced phosphatidylinositol-3-kinase (PI3K) signaling. In addition, metformin deactivates the downstream signaling molecules ERK and STAT3, which have effects on cell growth and apoptosis (8,12,13). IGF-1, insulin-like growth factor 1; ACC, acetyl-CoA carboxylase; HMG-CoA, 3-hydroxy-3-methyl-glutaryl-coenzyme A; p53, tumor protein p53; AKT, serine/theonine-specific protein kinase; ERK, extracellular signal-regulated kinase; TSC2, tuberous sclerosis complex 2; STAT3, signal transducer and activator of transcription 3.
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