ArticleCancer biology & therapy2017
The codon 72 polymorphism of p53 influences cell fate following nutrient deprivation.
Article in Cancer biology & therapy, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed, 27 citations in OpenAlex.
- Unbiased assessment of APR-246 responsive p53 mutants in ovarian cancer.Cell death discovery · 2026Article
- Adipocyte p53 coordinates the response to intermittent fasting by regulating adipose tissue immune cell landscape.Nature communications · 2024Article
- Association of the rs1042522 SNP with prostate cancer risk: a study of cancer tissues, primary tumor cultures, and serum samples from a Spanish Caucasian population.Frontiers in oncology · 2024Article
- Emerging insights into ethnic-specific TP53 germline variants.Journal of the National Cancer Institute · 2023Review
- It's Getting Complicated-A Fresh Look at p53-MDM2-ARF Triangle in Tumorigenesis and Cancer Therapy.Frontiers in cell and developmental biology · 2022Review
- Effect of the p53 P72R Polymorphism on Mutant TP53 Allele Selection in Human Cancer.Journal of the National Cancer Institute · 2021Article
- SARS-CoV-2: Understanding the Transcriptional Regulation of ACE2 and TMPRSS2 and the Role of Single Nucleotide Polymorphism (SNP) at Codon 72 of p53 in the Innate Immune Response against Virus Infection.International journal of molecular sciences · 2021Review
- Review
- The Codon 72Molecular cancer research : MCR · 2019Article
- Taking up the reins of power: metabolic functions of p53.Journal of molecular cell biology · 2019Review
- Common genetic variants in the TP53 pathway and their impact on cancer.Journal of molecular cell biology · 2019Review
- Tumor cells containing the African-Centric S47 variant ofOncotarget · 2019Article
- Control of metabolism by p53 - Cancer and beyond.Biochimica et biophysica acta. Reviews on cancer · 2018Review
- p53 as a Dichotomous Regulator of Liver Disease: The Dose Makes the Medicine.International journal of molecular sciences · 2018Review
- Mutant p53 controls tumor metabolism and metastasis by regulating PGC-1α.Genes & development · 2018Article
- TP53 codon 72 Polymorphism and bladder cancer risk: a meta-analysis and emphasis on the role of tumor or smoking status.Journal of Cancer · 2018Article
- The Role of RNA Editing in Cancer Development and Metabolic Disorders.Frontiers in endocrinology · 2018Review
- The p53 Tumor Suppressor in the Control of Metabolism and Ferroptosis.Frontiers in endocrinology · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The TP53 gene is distinguished as the most frequently mutated gene in cancer. Unlike most cancer-relevant genes, the TP53 gene is also distinguished by the existence of coding region polymorphisms that alter p53 sequence, and in some cases, also alter p53 function. A common coding region variant at amino acid 72 of p53 encodes either proline (P72) or arginine (R72). P72 is the ancestral variant and is most common in populations near the equator. The frequency of the R72 variant increases in a linear manner with latitude. To date, why the R72 variant arose in humans and was possibly selected for has remained unclear. Here-in we show that this single nucleotide polymorphism (SNP) influences the phosphorylation of p53 and the transactivation of the key p53 target CDKN1A (p21) specifically in response to nutrient deprivation, but not in response to conventional cytotoxic agents. Following activation of the kinase AMPK, R72 cells show increased phosphorylation on serine-15 and increased transactivation of the cyclin-dependent kinase inhibitor CDKN1A (p21) and the metabolic response genes PPARGC1B (PGC-1β) and PRKAB2 (AMPK-β2). This is accompanied by increased growth arrest and decreased apoptosis in R72 cells compared with P72 cells. The combined data fit best with the hypothesis that the R72 polymorphism confers increased cell survival in response to nutrient deprivation. This differential response to nutrient deprivation may explain part of selection for this SNP at northern latitudes, where nutrient deprivation might have been more frequent.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.