Abstract
A delicate balance in the levels of proteins that regulate the p53 tumor suppressor pathway exists such that subtle changes alter p53 tumor suppressor activity and cancer risk. Many single-nucleotide polymorphisms (SNPs) in the p53 pathway alter p53 transcriptional activity and are associated with cancer risk. In addition, some SNPs influence the gain-of-function (GOF) activities of mutant p53 through unknown mechanisms. In this issue of Genes & Development, Basu and colleagues (pp. 230–243) provide direct evidence that the presence of an R72 polymorphism enhances the GOF invasive and metastatic properties of mutant p53 by regulating interactions with PGC-1α, an important regulator of mitochondrial biogenesis and oxidative phosphorylation. The study culminates with evidence that R72 is associated with worse outcomes in human breast cancer.
Original language | English (US) |
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Pages (from-to) | 195-196 |
Number of pages | 2 |
Journal | Genes and Development |
Volume | 32 |
Issue number | 3-4 |
DOIs | |
State | Published - Feb 1 2018 |
Keywords
- Codon 72
- Metastasis
- Mutant p53
- Oxidative phosphorylation
- PGC-1α
ASJC Scopus subject areas
- Genetics
- Developmental Biology