Understanding the complex-I-ty of metformin action: limiting mitochondrial respiration to improve cancer therapy
Name
s12915-014-0082-4.pdf
Size
819.49 KB
Format
Adobe PDF
Checksum (MD5)
aa948786c881d3b42935959dbc10fb26
Author(s)
Luengo, Alba
Sullivan, Lucas Bryan
Vander Heiden, Matthew G.
Date Issued
October 2014
Journal
BMC Biology
Publisher
BioMed Central Ltd
Citation
Luengo, Alba, Lucas B Sullivan, and Matthew G Vander Heiden. “Understanding the Complex-I-Ty of Metformin Action: Limiting Mitochondrial Respiration to Improve Cancer Therapy.” BMC Biology 12, no. 1 (October 24, 2014).
Version
Final published version
Abstract
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.
MIT Department
Massachusetts Institute of Technology. Department of Biology
Koch Institute for Integrative Cancer Research at MIT
Terms of Use
Creative Commons Attribution
Persistent DSpace Link
DOI of Published Version
https://doi.org/10.1186/s12915-014-0082-4
