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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...
Formato: | Online Artículo Texto |
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Lenguaje: | English |
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中国肺癌杂志编辑部
2013
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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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collection | PubMed |
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. |
format | Online Article Text |
id | pubmed-6000667 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
publisher | 中国肺癌杂志编辑部 |
record_format | MEDLINE/PubMed |
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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