Inhibition of the carcinogenic effect of 7,12-dimethylbenz(a)anthracene in female rats by buformin, phenytoin, pineal polypeptide extract, and L-dopa

Anisimov, V. N.; Остроумова, М Н; Dil'man, V. M.

doi:10.1007/bf00836263

Cited by 15 publications

(10 citation statements)

References 3 publications

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“…More recently, abnormalities in these essential biological systems have been associated with an increased incidence of human cancer. [1][2][3][4][5][6][7] While the treatment of these important host factors is typically multifactorial and complex, there is some evidence that the anti-diabetic biguanide drug metformin (1,1-dimethylbiguanide hydrochloride) reduces the incidence of several types of cancers, including breast cancer. Like obesity and diabetes, breast cancer is both highly prevalent and morbid and there is significant overlap in the affected patient populations.…”

Section: Introductionmentioning

confidence: 99%

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Metformin inhibits breast cancer cell growth, colony formation and induces cell cycle arrest in vitro

Alimova

Fan²,

Edgerton³

et al. 2009

Cell Cycle

469

350

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The anti-diabetic drug metformin reduces human cancer incidence and improves the survival of cancer patients, including those with breast cancer. We studied the activity of metformin against diverse molecular subtypes of breast cancer cell lines in vitro. Metformin showed biological activity against all estrogen receptor (ER) positive and negative, erbB2 normal and abnormal breast cancer cell lines tested. It inhibited cellular proliferation, reduced colony formation and caused partial cell cycle arrest at the G(1) checkpoint. Metformin did not induce apoptosis (as measured by DNA fragmentation and PARP cleavage) in luminal A, B or erbB2 subtype breast cancer cell lines. At the molecular level, metformin treatment was associated with a reduction of cyclin D1 and E2F1 expression with no changes in p27(kip1) or p21(waf1). It inhibited mitogen activated protein kinase (MAPK) and Akt activity, as well as the mammalian target of rapamycin (mTOR) in both ER positive and negative, erbB2-overexpressing and erbB2-normal expressing breast cancer cells. In erbB2-overexpressing breast cancer cell lines, metformin reduced erbB2 expression at higher concentrations, and at lower concentrations within the therapeutic range, it inhibited erbB2 tyrosine kinase activity evidenced by a reduction of phosphorylated erbB2 (P-erbB2) at both auto- and Src- phosphorylation sites. These data suggest that metformin may have potential therapeutic utility against ER positive and negative, erbB2-overexpressing and erbB2-normal expressing breast cancer cells.

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Section: Introductionmentioning

confidence: 99%

“…22,23 Metformin and related compounds, which include phenformin (1-phenylethylbiguanide), buformin (N-butylbiguanide), that counterbalance aberrant glucose metabolism have been shown to inhibit mammary tumorigenesis in rodent models (spontaneous or carcinogen induced) as well. [1][2][3][4][5][6][7]24 Metformin has most recently been shown…”

Section: Introductionmentioning

confidence: 99%

Metformin inhibits breast cancer cell growth, colony formation and induces cell cycle arrest in vitro

Alimova

Fan²,

Edgerton³

et al. 2009

Cell Cycle

469

350

View full text Add to dashboard Cite

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“…The anticarcinogenic effect of antidiabetic biguanides has been demonstrated in several models of induced carcinogenesis (Table 2). Daily oral administration of phenformin or buformin suppressed DMBA‐induced mammary tumor development in rats 93,94,96. Phenformin‐treated rats revealed a tendency toward a decrease in serum insulin level.…”

Section: Effect Of Antidiabetic Drugs On Carcinogenesismentioning

confidence: 93%

“…Daily oral administration of phenformin or buformin suppressed DMBA-induced mammary tumor development in rats. 93,94,96 Phenformin-treated rats revealed a tendency toward a decrease in serum insulin level. The treatment with phenformin normalized the tolerance to glucose and serum insulin and IGF-1 level in rats exposed to intravenous injections of N-nitrosomethylurea (NMU) and inhibited mammary carcinogenesis in these animals.…”

Section: Effect Of Antidiabetic Drugs On Carcinogenesismentioning

confidence: 95%

Central and Peripheral Effects of Insulin/IGF‐1 Signaling in Aging and Cancer: Antidiabetic Drugs as Geroprotectors and Anticarcinogens

Anisimov

Berstein

Popovich

et al. 2005

Annals of the New York Academy of Sciences

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Studies in mammals have led to the suggestion that hyperglycemia and hyperinsulinemia are important factors both in aging and in the development of cancer. Insulin/insulin-like growth factor 1 (IGF-1) signaling molecules linked to longevity include DAF-2 and insulin receptor (InR) and their homologues in mammals and to inactivation of the corresponding genes followed by increased life span in nematodes, fruit flies, and mice. It is possible that the life-prolonging effect of caloric restriction are due to decreasing IGF-1 levels. A search of pharmacological modulators of life span-extending mutations in the insulin/IGF-1 signaling pathway and mimetics of effects of caloric restriction could be a direction in the regulation of longevity. Some literature and our own observations suggest that antidiabetic drugs could be promising candidates for both life span extension and prevention of cancer.

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“…Так, при длительном применении метформина у самок мышей линии С3Н/SH отмечали торможение роста спонтанных аденокарцином в 4 раза [6], угнетение развития спонтанных опухолей у крыс -в 1,6 раза [7,8]. Ежедневное применение метформина угнетало возникновение опухолей после введения канцерогенов у мышей и крыс, в том числе опухолей грудной железы у крыс при введении бензантрацена или нитрозометилмочевины [9][10][11]. Метформин ингибировал рост аденокарциномы кишечника у крыс после введения им диметилгидразина, а также нормализовал уровень глюкозы, инсулина, триглицеридов, повышал иммунный статус, сниженный при действии канцерогена [10][11][12].…”

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The metformin influence on proliferation cells of brain tumor in cell culture in vitro

et al. 2012

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Влияние метôормина на пролиôерациþ клеток опухолей головного мозга в культуре клеток in vitro Вступление. В настоящее время исследователи уделяют большое внимание изучению противоопухолевого действия антидиабетического препарата метформин на различные опухоли человека, в том числе опухоли мозга. Целью работы было изучение влияния метформина на глиальные опухоли в культуре клеток in vitro. Материалы и методы. Антипролиферативное и цитотоксическое действие метформина на различные опухоли головного мозга изучено в культуре клеток in vitro в течение 24 ч при температуре 37°С с помощью 0,1% раствора трипанового синего. Исследованы 26 опухолей головного мозга различного происхождения. Результаты. Противодиабетический препарат метформин оказывал антипролиферативное и цитотоксическое действие на клетки различных опухолей головного мозга в суспензионной культуре клеток in vitro. Противоопухолевый эффект зависел от дозы препарата, большие дозы-100 мкг/мл более эффективны, чем малые-1 мкг/мл. Злокачественные глиомы головного мозга (глиобластомы) более чувствительны к действию метформина, чем астроцитомы I-II степени анаплазии. Выводы. Полученные данные позволяют рекомендовать использование метформина у нейроонкологических больных на этапах комбинированного лечения.

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Inhibition of the carcinogenic effect of 7,12-dimethylbenz(a)anthracene in female rats by buformin, phenytoin, pineal polypeptide extract, and L-dopa

Cited by 15 publications

References 3 publications

Metformin inhibits breast cancer cell growth, colony formation and induces cell cycle arrest in vitro

Metformin inhibits breast cancer cell growth, colony formation and induces cell cycle arrest in vitro

Central and Peripheral Effects of Insulin/IGF‐1 Signaling in Aging and Cancer: Antidiabetic Drugs as Geroprotectors and Anticarcinogens

The metformin influence on proliferation cells of brain tumor in cell culture in vitro

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