Understanding the complex-I-ty of metformin action: limiting mitochondrial respiration to improve cancer therapy

BMC Biology

Commentary

Lucas B Sullivan¹  Alba Luengo¹  Matthew G Vander Heiden² 

[1] The Koch Institute for Integrative Cancer Research and Department of Biology, Massachusetts Institute of Technology, 02139, Cambridge, MA, USA;The Koch Institute for Integrative Cancer Research and Department of Biology, Massachusetts Institute of Technology, 02139, Cambridge, MA, USA;Dana-Farber Cancer Institute, 02115, Boston, MA, USA;

关键词: Metformin;    AMPK Activation;    Metformin Treatment;    Mitochondrial Electron Transport Chain;    Increase Blood Glucose;   

DOI  :  10.1186/s12915-014-0082-4

来源: Springer

【 摘 要 】

Metformin has been a first-line treatment for type II diabetes mellitus for decades and is the most widely prescribed antidiabetic drug. Retrospective studies have found that metformin treatment is associated with both reduced cancer diagnoses and cancer-related deaths. Despite the prevalence of metformin use in the clinic, its molecular mechanism of action remains controversial. In a recent issue of Cancer & Metabolism, Andrzejewski et al. present evidence that metformin acts directly on mitochondria to inhibit complex I and limits the ability of cancer cells to cope with energetic stress. Here, we discuss evidence that supports the role of metformin as a cancer therapeutic.See research article: http://www.cancerandmetabolism.com/content/2/1/12.

【 授权许可】

Unknown   
© Luengo et al.; licensee BioMed Central Ltd. 2014. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.