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Review
. 2022 Oct 25;23(21):12893.
doi: 10.3390/ijms232112893.

Metformin Improves Ovarian Cancer Sensitivity to Paclitaxel and Platinum-Based Drugs: A Review of In Vitro Findings

Affiliations
Review

Metformin Improves Ovarian Cancer Sensitivity to Paclitaxel and Platinum-Based Drugs: A Review of In Vitro Findings (V体育平台登录)

Giovanni Tossetta. Int J Mol Sci. .

Abstract

Ovarian cancer is one of the most dangerous gynecologic cancers worldwide, showing a high fatality rate and recurrence due to diagnosis at an advanced stage of the disease and the occurrence of chemoresistance, which weakens the therapeutic effects of the chemotherapeutic treatments. In fact, although paclitaxel and platinum-based drugs (carboplatin or cisplatin) are widely used alone or in combination to treat ovarian cancer, the occurrence of chemoresistance significantly reduces the effects of these drugs. Metformin is a hypoglycemic agent that is commonly used for the treatment of type 2 diabetes mellitus and non-alcoholic fatty liver disease. However, this drug also shows anti-tumor activity, reducing cancer risk and chemoresistance. This review analyzes the current literature regarding the role of metformin in ovarian cancer and investigates what is currently known about its effects in reducing paclitaxel and platinum resistance to restore sensitivity to these drugs VSports手机版. .

Keywords: chemotherapy; metformin; ovarian cancer; paclitaxel; platinum; resistance V体育安卓版. .

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Conflict of interest statement

The author declares no conflict of interest.

"VSports最新版本" Figures

Figure 1
Figure 1
Chemical structures of paclitaxel, carboplatin, cisplatin, and metformin.
Figure 2
Figure 2
Schematic representation of metformin’s effects on ovarian cancer cells. Tunneling nanotube (TNT); Insulin-like growth factor 1 (IGF-1); IGF-1 receptor (IGF1R); Small nucleolar RNA hostgene 7 (SNHG7); Multidrug resistance-associated protein 2 (MRP2); Extracellular signal-regulated kinase 1/2 (ERK1/2); phospho-AKT (pAKT); nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB); Vascular endothelial growth factor (VEGF); Hexokinase II (HKII); phosphor- pyruvate dehydrogenase kinase-1 (pPDK1); B-cell lymphoma 2 (Bcl-2); Bcl-2-associated X (Bax); mechanistic target of rapamycin (mTOR).

"V体育2025版" References

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