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Metformin and ovarian cancer: the evidence
Elina Urpilainen1, Ulla Puistola1, Stergios Boussios2,3
1Department of Obstetrics and Gynaecology, PEDEGO Research Unit, Medical Research Center Oulu, University of Oulu and University Hospital of Oulu, Oulu, Finland.
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.
Insights
Metformin shows preclinical anticancer effects in ovarian cancer by inhibiting mitochondrial respiration and lowering growth factors. However, clinical evidence is less promising, possibly due to higher concentrations used in preclinical studies.
Area of Science:
- Oncology
- Pharmacology
- Biochemistry
Background:
- Metformin, an antidiabetic drug, exhibits broad signaling pathway effects with few side effects and low cost.
- Preclinical studies demonstrate dose-dependent anticancer effects of metformin, including direct inhibition of mitochondrial respiratory chain complex I and indirect effects via metabolic modulation.
- Metformin has shown chemosensitizing properties and angiogenesis inhibition in ovarian cancer models.
Purpose of the Study:
- To review and evaluate the preclinical and clinical evidence for metformin's efficacy in ovarian cancer treatment.
- To assess the discrepancy between promising preclinical findings and less conclusive clinical outcomes.
- To discuss the potential impact of varied metformin concentrations on clinical utility.
Main Methods:
- Literature review of preclinical (in vitro and in vivo) studies on metformin's anticancer effects in ovarian cancer.
- Analysis of epidemiological studies investigating metformin use in ovarian cancer patients.
- Evaluation of dose-dependency and concentration differences between preclinical and clinical settings.
Main Results:
- Preclinical data indicate significant anticancer effects, including chemosensitization and anti-angiogenesis, in ovarian cancer.
- Epidemiological studies on metformin in ovarian cancer have yielded less promising results compared to preclinical data.
- A key discrepancy lies in the higher metformin concentrations used in preclinical research versus clinical pharmacological doses.
Conclusions:
- Metformin exhibits promising preclinical anticancer activity in ovarian cancer, targeting key cellular pathways.
- Clinical evidence supporting metformin's efficacy in ovarian cancer is currently limited and requires further investigation.
- The translation of preclinical findings to clinical practice may be hindered by differences in metformin dosage and concentration.
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