[Metformin and malignant neoplasms: a possible mechanism of antitumor action and prospects for use in practice].

Q4 Medicine
K O Kuznetsov, E R Safina, D V Gaimakova, Ya S Frolova, I Yu Oganesyan, A G Sadertdinova, K A Nazmieva, A H Islamgulov, A R Karimova, A M Galimova, E V Rizvanova
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引用次数: 0

Abstract

Metformin is a first-line antidiabetic drug for the treatment of type 2 diabetes mellitus (DM2); its molecular target is AMP-activated protein kinase (AMPK), which is involved in many metabolic processes. Metformin not only reduces blood glucose levels and improves insulin sensitivity, but also inhibits lipolysis and reduces cardiovascular risk in patients with DM2. In recent years, it has been proven that metformin slows down the aging process, stimulates hair growth, eliminates cognitive impairment, and also has an antitumor effect. Most basic studies have shown that metformin inhibits the growth of tumor cells and promotes cellular apoptosis, while clinical studies show contradictory results. This discrepancy can be explained by the difference in the concentration of metformin between basic and clinical studies. The maximum daily dose of metformin for patients with DM2 is 2500 mg / day, and the dose used in basic research was much higher. Metformin directly activates the AMPK signaling pathway, inhibits the production of reactive oxygen species, induces the activation of mTORC1, inhibits cyclin D1, which leads to a reduction in the risk of the occurrence and development of malignant neoplasms. In addition, metformin indirectly inhibits tumor growth, proliferation, invasion and metastasis by reducing the concentration of glucose in the blood, insulin resistance, as well as by reducing inflammation and affecting the tumor microenvironment. Glycolysis plays an important role in the energy metabolism of tumors, and metformin is able to have an inhibitory effect on it. Currently, studies of the mechanism of antitumor effects of metformin are becoming more extensive and in-depth, but there are still some contradictions.

[二甲双胍与恶性肿瘤:抗肿瘤作用的可能机制及实际应用前景]。
二甲双胍是治疗 2 型糖尿病(DM2)的一线抗糖尿病药物;其分子靶点是 AMP 激活蛋白激酶(AMPK),AMPK 参与许多代谢过程。二甲双胍不仅能降低血糖水平,改善胰岛素敏感性,还能抑制脂肪分解,降低 DM2 患者的心血管风险。近年来的研究证明,二甲双胍能延缓衰老,刺激毛发生长,消除认知障碍,还具有抗肿瘤作用。大多数基础研究表明,二甲双胍可抑制肿瘤细胞的生长,促进细胞凋亡,而临床研究却显示出相互矛盾的结果。造成这种差异的原因是基础研究和临床研究中二甲双胍的浓度不同。二甲双胍对 DM2 患者的最大日剂量为 2500 毫克/天,而基础研究中使用的剂量要高得多。二甲双胍可直接激活 AMPK 信号通路,抑制活性氧的产生,诱导 mTORC1 的激活,抑制细胞周期蛋白 D1,从而降低恶性肿瘤发生和发展的风险。此外,二甲双胍还能通过降低血液中的葡萄糖浓度、胰岛素抵抗以及减少炎症和影响肿瘤微环境,间接抑制肿瘤的生长、增殖、侵袭和转移。糖酵解在肿瘤的能量代谢中起着重要作用,而二甲双胍能够对其产生抑制作用。目前,对二甲双胍抗肿瘤作用机制的研究越来越广泛和深入,但仍存在一些矛盾。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Problemy endokrinologii
Problemy endokrinologii Medicine-Endocrinology, Diabetes and Metabolism
CiteScore
1.40
自引率
0.00%
发文量
59
期刊介绍: Since 1955 the “Problems of Endocrinology” (or “Problemy Endocrinologii”) Journal publishes timely articles, balancing both clinical and experimental research, case reports, reviews and lectures on pressing problems of endocrinology. The Journal is aimed to the most topical issues of endocrinology: to chemical structure, biosynthesis and metabolism of hormones, the mechanism of their action at cellular and molecular level; pathogenesis and to clinic of the endocrine diseases, new methods of their diagnostics and treatment. The Journal: features original national and foreign research articles, reflecting world endocrinology development; issues thematic editions on specific areas; publishes chronicle of major international congress sessions and workshops on endocrinology, as well as state-of-the-art guidelines; is intended for scientists, endocrinologists diabetologists and specialists of allied trade, general practitioners, family physicians and pediatrics.
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