Title
Mitochondrial dysfunction in cancer: Potential roles of ATF5 and the mitochondrial UPR
UMMS Affiliation
Department of Molecular, Cell and Cancer Biology; UMass Metabolic Network
Publication Date
5-10-2017
Document Type
Article
Disciplines
Biochemistry | Cell Biology | Cellular and Molecular Physiology | Molecular Biology
Abstract
Mitochondria form a cellular network of organelles, or cellular compartments, that efficiently couple nutrients to energy production in the form of ATP. As cancer cells rely heavily on glycolysis, historically mitochondria and the cellular pathways in place to maintain mitochondrial activities were thought to be more relevant to diseases observed in non-dividing cells such as muscles and neurons. However, more recently it has become clear that cancers rely heavily on mitochondrial activities including lipid, nucleotide and amino acid synthesis, suppression of mitochondria-mediated apoptosis as well as oxidative phosphorylation (OXPHOS) for growth and survival. Considering the variety of conditions and stresses that cancer cell mitochondria may incur such as hypoxia, reactive oxygen species and mitochondrial genome mutagenesis, we examine potential roles for a mitochondrial-protective transcriptional response known as the mitochondrial unfolded protein response (UPRmt) in cancer cell biology.
Keywords
ATF5, Cancer, Mitochondria, UPR(mt)
DOI of Published Version
10.1016/j.semcancer.2017.05.002
Source
Semin Cancer Biol. 2017 May 10. pii: S1044-579X(17)30125-6. doi: 10.1016/j.semcancer.2017.05.002. [Epub ahead of print] Link to article on publisher's site
Journal/Book/Conference Title
Seminars in cancer biology
Related Resources
PubMed ID
28499833
Repository Citation
Deng, Pan and Haynes, Cole M., "Mitochondrial dysfunction in cancer: Potential roles of ATF5 and the mitochondrial UPR" (2017). UMass Metabolic Network Publications. 115.
https://escholarship.umassmed.edu/metnet_pubs/115