Abstract

The results of preclinical, epidemiological and clinical studies have shown that metformin, the main drug used in the treatment of type 2 diabetes, has antitumor activity. Metformin reduces the incidence of malignant neoplasms in various locations, including gynaecological tumours. It lowers morbidity, has a positive effect on the course of the disease and reduces mortality. The mechanism of the antitumor action of metformin is pleiotropic and involves several signalling pathways, including AMPK/mTOR (mitogen activated protein kinase/mammalian target rapamycin), STAT3 (signal transducer and activator of transcription) and numerous factors: NF-KB (nuclear factor kappa), HIF-1 alpha (hypoxia inducible factor 1), IGF-1 (insulin-like growth factor-1), which affect cell proliferation and apoptosis. In addition, metformin eliminates CSCs (cancer stem cells) that are associated with cancer progression, metastasis and resistance to treatment. The effect of metformin in breast and endometrial cancer is favourable in the vast majority of studies. The results of studies on ovarian and cervical cancer promote metformin as a candidate in the combination treatment of these cancers. More results from meta-analyzes and clinical trials are awaited. It is clearly recognized that metformin as an antidiabetic in women with type 2 diabetes has an advantage over other antidiabetics due to its anticancer activity.

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