Abstract
Recent evidence in humans and mice supports the notion that mitochondrial metabolism is active and necessary for tumor growth. Mitochondrial metabolism supports tumor anabolism by providing key metabolites for macromolecule synthesis and generating oncometabolites to maintain the cancer phenotype. Moreover, there are multiple clinical trials testing the efficacy of inhibiting mitochondrial metabolism as a new cancer therapeutic treatment. In this review, we discuss the rationale of using these anti-cancer agents in clinical trials and highlight how to effectively utilize them in different tumor contexts.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 341-352 |
| Number of pages | 12 |
| Journal | Cell Metabolism |
| Volume | 32 |
| Issue number | 3 |
| DOIs | |
| State | Published - Sep 1 2020 |
Funding
This work was supported by the NIH ( 5R35CA197532 ) to N.S.C. and the NIH ( 5T32CA9560-33 ) to K.V. and Northwestern University Pulmonary and Critical Care Department’s Cugell Fellowship to K.V. We thank Hyewon Kong and Colleen Reczek for their input in the CRISPR screen. Figures created with https://biorender.com/ . This work was supported by the NIH (5R35CA197532) to N.S.C. and the NIH (5T32CA9560-33) to K.V. and Northwestern University Pulmonary and Critical Care Department's Cugell Fellowship to K.V. We thank Hyewon Kong and Colleen Reczek for their input in the CRISPR screen. Figures created with https://biorender.com/. N.S.C. is an SAB member of Raphael Pharmaceuticals (Devimistat – CPI-613).
Keywords
- metformin
- mitochondria
ASJC Scopus subject areas
- Physiology
- Molecular Biology
- Cell Biology
