Regulation of nucleotide metabolism by mutant p53 contributes to its gain-of-function activities
Open accessAbstract
Mutant p53 (mtp53) is an oncogene that drives cancer cell proliferation. Here we report that mtp53 associates with the promoters of numerous nucleotide metabolism genes (NMG). Mtp53 knockdown reduces NMG expression and substantially depletes nucleotide pools, which attenuates GTP-dependent protein activity and cell invasion. Addition of exogenous guanosine or GTP restores the invasiveness of mtp53 knockdown cells, suggesting that mtp53 promotes invasion by increasing GTP. In addition, mtp53 creates a dependency on the nucleoside salvage pathway enzyme deoxycytidine kinase for the maintenance of a proper balance in dNTP pools required for proliferation. These data indicate that mtp53-harbouring cells have acquired a synthetic sick or lethal phenotype relationship with the nucleoside salvage pathway. Finally, elevated expression of NMG correlates with mutant p53 status and poor prognosis in breast cancer patients. Thus, mtp53’s control of nucleotide biosynthesis has both a driving and sustaining role in cancer development. Mutations in the tumour suppressor p53 can produce a protein that has additional functions. Here, the authors describe gain of function mutants of p53 that induce the expression of genes involved in nucleotide metabolism, which increases the activity of GTPases and results in invasion and metastasis.
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Mutant p53 alleles facilitate expression of nucleotide biosynthesis genes including IMPDH1/2, GMPS, DCK, and TK1.
“Besides the regulatory inputs from c-myc, mutant p53 alleles have also been shown to facilitate expression of nucleotide biosynthesis genes, among which are IMPDH1 and 2, GMP synthetase (GMPS) and nucleoside salvage enzymes deoxycytidine kinase (DCK) and thymidine kinase (TK1) (Kollareddy et al., 2015).”
From The emerging hallmarks of cancer metabolism (2016) · cites this paper as Kollareddy et al., 2015
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- Authors
- Kollareddy, M., Dimitrova, E., Vallabhaneni, K. C., Chan, A., Le, T., Chauhan, K. M., Carrero, Z. I., Ramakrishnan, G., Watabe, K., Haupt, Y., Haupt, S., Pochampally, R., Boss, G. R., Romero, D. G., Radu, C. G., & Martinez, L. A.
- Affiliations
- University of California, Los Angeles (US)
- University of Mississippi Medical Center (US)
- University of California San Diego (US)
- The University of Melbourne (AU)
- Corresponding author
- Martinez, Luis A.
- ORCID
- Venue
- Nature Communications
- Published
- 2015-06-12
- Volume
- 6
- Issue
- 1
- Pages
- 7389-7389
- ISSN
- 2041-1723 (ISSN-L)
- PMC
- PMC4467467
- OpenAlex
- W2266420598
- Cited by
- 127
- References
- 63
- Citations by year
- 2026: 6 · 2025: 6 · 2024: 11 · 2023: 12 · 2022: 11 · 2021: 14 · 2020: 9 · 2019: 14 · 2018: 18 · 2017: 12 · 2016: 12 · 2015: 2
- FWCI
- 6.41
- Type
- journal article
- Language
- en
- Update notices
- correction (2026-02-03)
- Open access
- gold
- doi.org
- Licence
- Locations
- Nature Communications (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Explore Bristol Research (submittedVersion, other-oa)
- RePEc: Research Papers in Economics (submittedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Minerva Access (University of Melbourne) (submittedVersion)
- Bristol Research (University of Bristol) (submittedVersion, other-oa)
- Funders
- National Cancer Institute (CA166974-01A1, R01CA173499, R01CA166974, P30CA016042)
- Topics
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Biochemical and Molecular Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
- Keywords
- mutant p53, gain-of-function p53, nucleotide metabolism, nucleotide synthesis, GTP, nucleoside salvage pathway, deoxycytidine kinase, dNTP pools, cell invasion, metastasis, breast cancer, synthetic lethality, GTPase
- MeSH terms
- Animals, Brain Neoplasms, Breast Neoplasms, Cell Cycle, Deoxycytidine Kinase, Female, Guanosine Triphosphate, Humans, Mutation, Neoplasm Invasiveness, Neoplasm Transplantation, Nucleosides, Nucleotides, Prognosis, Promoter Regions, Genetic, Tumor Stem Cell Assay, Blotting, Western, Gene Expression Regulation, Neoplastic, Proportional Hazards Models, Tumor Suppressor Protein p53, Cell Line, Tumor, Immunoprecipitation, Cell Proliferation, Mice, Kaplan-Meier Estimate, Gene Knockdown Techniques
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