Metformin for aging and cancer prevention

Anisimov, Vladimir N.

doi:10.18632/aging.100230

Cited by 132 publications

(116 citation statements)

References 129 publications

(181 reference statements)

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“…Metformin postponed spontaneous carcinogenesis in mice and rats, as well as chemical and radiation carcinogenesis in mice, rats, and hamsters (45). In addition, in female SHR mice, metformin increased life span and postponed tumors when started at young or middle age but not when started at old age (46).…”

Section: Pycontrolmentioning

confidence: 91%

The Antidiabetic Drug Metformin Inhibits Gastric Cancer Cell Proliferation In Vitro and In Vivo

Kato

Iwama

et al. 2012

Molecular Cancer Therapeutics

211

199

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Recent studies suggest that metformin, which is commonly used as an oral anti-hyperglycemic agent of the biguanide family, may reduce cancer risk and improve prognosis, but the mechanisms by which metformin affects various cancers, including gastric cancer, remains unknown. The goal of the present study was to evaluate the effects of metformin on human gastric cancer cell proliferation in vitro and in vivo and to study microRNAs (miRNA) associated with antitumor effect of metformin. We used MKN1, MKN45, and MKN74 human gastric cancer cell lines to study the effects of metformin on human gastric cancer cells. Athymic nude mice bearing xenograft tumors were treated with or without metformin. Tumor growth was recorded after 4 weeks, and the expression of cell-cycle-related proteins was determined. In addition, we used miRNA array tips to explore the differences among miRNAs in MKN74 cells bearing xenograft tumors treated with or without metformin in vitro and in vivo. Metformin inhibited the proliferation of MKN1, MKN45, and MKN74 in vitro. Metformin blocked the cell cycle in G 0 -G 1 in vitro and in vivo. This blockade was accompanied by a strong decrease of G 1 cyclins, especially in cyclin D1, cyclin-dependent kinase (Cdk) 4, Cdk6 and by a decrease in retinoblastoma protein (Rb) phosphorylation. In addition, metformin reduced the phosphorylation of epidermal growth factor receptor and insulin-like growth factor-1 receptor in vitro and in vivo. The miRNA expression was markedly altered with the treatment of metformin in vitro and in vivo. Various miRNAs altered by metformin also may contribute to tumor growth in vitro and in vivo. Mol Cancer Ther; 11(3); 549-60. Ó2012 AACR.

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Section: Pycontrolmentioning

confidence: 91%

The Antidiabetic Drug Metformin Inhibits Gastric Cancer Cell Proliferation In Vitro and In Vivo

Kato

Iwama

et al. 2012

Molecular Cancer Therapeutics

211

199

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“…24 There is an exponential growth of publications on reduced risk of cancer and cardiovascular diseases in patients treated with metformin. 3,[25][26][27][28] Antidiabetic biguanides seem to be more effective than caloric restriction and some of the genetic manipulations in preventing age-related deterioration of insulin levels. 3 It remains to be shown whether antidiabetic biguanides extend lifespan independently of calorie restriction (CR).…”

mentioning

confidence: 99%

Metformin: Do we finally have an anti-aging drug?

Anisimov

2013

Cell Cycle

Self Cite

108

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“…Noteworthy, metformin, which affects the AMPK/mTOR pathway, also extends life span in mice and prevents cancer in mice [41][42][43][44][45][46][47][48][49] Unlike metformin, which is effective mostly when started early in life, 45 rapamycin extends life span when the treatment started both in young and in old animals ( Table 4). In order to develop low-dose anti-aging therapy for humans, one needs to determine the minimum effective dose of rapamycin.…”

Section: Discussionmentioning

confidence: 99%