Is Reliance on Mitochondrial Respiration a “Chink in the Armor” of Therapy-Resistant Cancer?

A series of recent reports has suggested PGC1α-driven upregulation of mitochondrial oxidative phosphorylation as a selective vulnerability of drug-resistant cancers. Accordingly, chemical inhibitors of respiration led to selective eradication of such cancer cells due to their preferential sensitivit...

Full description

Saved in:
Bibliographic Details
Published in:Cancer cell 2014-12, Vol.26 (6), p.788-795
Main Author: Wolf, Dieter A.
Format: Article
Language:English
Subjects:
Animals
Antineoplastic Agents - pharmacology
Drug Resistance, Neoplasm - drug effects
Humans
Mitochondria - metabolism
Neoplasms - drug therapy
Neoplasms - metabolism
Oxidative Phosphorylation - drug effects
Oxidative Stress - drug effects
Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha
Reactive Oxygen Species - metabolism
Transcription Factors - metabolism
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:A series of recent reports has suggested PGC1α-driven upregulation of mitochondrial oxidative phosphorylation as a selective vulnerability of drug-resistant cancers. Accordingly, chemical inhibitors of respiration led to selective eradication of such cancer cells due to their preferential sensitivity to mitochondrial production of reactive oxygen species. These insights create a timely opportunity for a biomarker guided application of already existing and newly emerging mitochondrial inhibitors in recurrent drug-resistant cancer, including lymphomas, melanomas, and other malignant diseases marked by increased mitochondrial respiration.
ISSN:1535-6108
1878-3686
DOI:10.1016/j.ccell.2014.10.001