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二甲双胍通过激活腺苷酸活化蛋白激酶(AMPK)的抗肿瘤机制

Metformin, as a traditional oral hypoglycemic agent, is commonly used in the clinical treatment for type 2 diabetes. Recently, a large number of epidemiological researches have shown that metformin could reduce the tumor morbidity of type 2 diabetes, moreover, it has also been indicated that metform...

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Detalles Bibliográficos
Formato: Online Artículo Texto
Lenguaje:English
Publicado: 中国肺癌杂志编辑部 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6000667/
https://www.ncbi.nlm.nih.gov/pubmed/23945247
http://dx.doi.org/10.3779/j.issn.1009-3419.2013.08.07
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description Metformin, as a traditional oral hypoglycemic agent, is commonly used in the clinical treatment for type 2 diabetes. Recently, a large number of epidemiological researches have shown that metformin could reduce the tumor morbidity of type 2 diabetes, moreover, it has also been indicated that metformin could inhibit the growth, proliferation and transformation of cancer cells in metabolic pathways, cell cycle, oxidative stress and cancer/tumor stem cells transformation via AMPK pathway activation. But the antitumor e?ect of metformin via AMPK activation still exists arguments, and the defnite mechanism remains to be further investigated and confrmed by extensive clinical trials.
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spelling pubmed-60006672018-07-06 二甲双胍通过激活腺苷酸活化蛋白激酶(AMPK)的抗肿瘤机制 Zhongguo Fei Ai Za Zhi 综述 Metformin, as a traditional oral hypoglycemic agent, is commonly used in the clinical treatment for type 2 diabetes. Recently, a large number of epidemiological researches have shown that metformin could reduce the tumor morbidity of type 2 diabetes, moreover, it has also been indicated that metformin could inhibit the growth, proliferation and transformation of cancer cells in metabolic pathways, cell cycle, oxidative stress and cancer/tumor stem cells transformation via AMPK pathway activation. But the antitumor e?ect of metformin via AMPK activation still exists arguments, and the defnite mechanism remains to be further investigated and confrmed by extensive clinical trials. 中国肺癌杂志编辑部 2013-08-20 /pmc/articles/PMC6000667/ /pubmed/23945247 http://dx.doi.org/10.3779/j.issn.1009-3419.2013.08.07 Text en 版权所有©《中国肺癌杂志》编辑部2013 https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed in accordance with the terms of the Creative Commons Attribution (CC BY 3.0) License. See: https://creativecommons.org/licenses/by/3.0/
spellingShingle 综述
二甲双胍通过激活腺苷酸活化蛋白激酶(AMPK)的抗肿瘤机制
title 二甲双胍通过激活腺苷酸活化蛋白激酶(AMPK)的抗肿瘤机制
title_full 二甲双胍通过激活腺苷酸活化蛋白激酶(AMPK)的抗肿瘤机制
title_fullStr 二甲双胍通过激活腺苷酸活化蛋白激酶(AMPK)的抗肿瘤机制
title_full_unstemmed 二甲双胍通过激活腺苷酸活化蛋白激酶(AMPK)的抗肿瘤机制
title_short 二甲双胍通过激活腺苷酸活化蛋白激酶(AMPK)的抗肿瘤机制
title_sort 二甲双胍通过激活腺苷酸活化蛋白激酶(ampk)的抗肿瘤机制
topic 综述
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6000667/
https://www.ncbi.nlm.nih.gov/pubmed/23945247
http://dx.doi.org/10.3779/j.issn.1009-3419.2013.08.07
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