ArticleMolecular oncology2016
A rare DNA contact mutation in cancer confers p53 gain-of-function and tumor cell survival via TNFAIP8 induction.
Article in Molecular oncology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 35 citations in OpenAlex.
- Splice-altering TP53 missense mutations as drivers of dysfunction and targets for RNA-based therapy.Stem cell research & therapy · 2026Article
- Lung cancer-enriched p53 mutants occupy canonical p53 target genes without activating transcription, revealing a distinct loss-of-function behavior.bioRxiv : the preprint server for biology · 2026Article
- Distinct functional heterogeneity of TP53 R175 mutations in platinum-resistant ovarian cancer: unveiling molecular mechanisms and therapeutic targets.Cell death & disease · 2025Article
- Unraveling the Guardian: p53's Multifaceted Role in the DNA Damage Response and Tumor Treatment Strategies.International journal of molecular sciences · 2024Review
- Antisense-mediated splicing correction as a therapeutic approach for p53 K120R mutation.BMB reports · 2024Article
- Kidney tubular epithelial cells control interstitial fibroblast fate by releasing TNFAIP8-encapsulated exosomes.Cell death & disease · 2023Article
- Mutant p53Frontiers in genetics · 2022Article
- MicroRNA-205-5p inhibits skin cancer cell proliferation and increase drug sensitivity by targeting TNFAIP8.Scientific reports · 2021Article
- The RanBP2/RanGAP1-SUMO complex gates β-arrestin2 nuclear entry to regulate the Mdm2-p53 signaling axis.Oncogene · 2021Article
- Distinct mechanisms control genome recognition by p53 at its target genes linked to different cell fates.Nature communications · 2021Article
- TNFAIP8 drives metabolic reprogramming to promote prostate cancer cell proliferation.The international journal of biochemistry & cell biology · 2021Article
- TNFAIP8 Promotes Cisplatin Chemoresistance in Triple-Negative Breast Cancer by Repressing p53-Mediated miR-205-5p Expression.Molecular therapy. Nucleic acids · 2020Article
- LncRNA H19 promotes triple-negative breast cancer cells invasion and metastasis through the p53/TNFAIP8 pathway.Cancer cell international · 2020Article
- Inhibition of Aurora A enhances radiosensitivity in selected lung cancer cell lines.Respiratory research · 2019Article
- Dual Targeting of EGFR and IGF1R in the TNFAIP8 Knockdown Non-Small Cell Lung Cancer Cells.Molecular cancer research : MCR · 2019Article
- Comparison of genotoxic versus nongenotoxic stabilization of p53 provides insight into parallel stress-responsive transcriptional networks.Cell cycle (Georgetown, Tex.) · 2019Article
- K120R mutation inactivates p53 by creating an aberrant splice site leading to nonsense-mediated mRNA decay.Oncogene · 2019Article
- Network-guided prediction of aromatase inhibitor response in breast cancer.PLoS computational biology · 2019Article
- TNFAIP8: Inflammation, Immunity and Human Diseases.Journal of cellular immunology · 2019Article
- Review
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
The p53 tumor suppressor gene encodes a sequence-specific transcription factor. Mutations in the coding sequence of p53 occur frequently in human cancer and often result in single amino acid substitutions (missense mutations) in the DNA binding domain (DBD), blocking normal tumor suppressive functions. In addition to the loss of canonical functions, some missense mutations in p53 confer gain-of-function (GOF) activities to tumor cells. While many missense mutations in p53 cluster at six "hotspot" amino acids, the majority of mutations in human cancer occur elsewhere in the DBD and at a much lower frequency. We report here that mutations at K120, a non-hotspot DNA contact residue, confer p53 with the previously unrecognized ability to bind and activate the transcription of the pro-survival TNFAIP8 gene. Mutant K120 p53 binds the TNFAIP8 locus at a cryptic p53 response element that is not occupied by wild-type p53. Furthermore, induction of TNFAIP8 is critical for the evasion of apoptosis by tumor cells expressing the K120R variant of p53. These findings identify induction of pro-survival targets as a mechanism of gain-of-function activity for mutant p53 and will likely broaden our understanding of this phenomenon beyond the limited number of GOF activities currently reported for hotspot mutants.
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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.