ArticleNature communications2021
The oncogenicity of tumor-derived mutant p53 is enhanced by the recruitment of PLK3.
Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 24 citations in OpenAlex.
- Oncogenic p53 induces mitotic errors in lung cancer cells by recopying DNA replication forks conferring targetable proliferation advantage.Cell death and differentiation · 2026Article
- p53: from understanding its structure to advances in therapeutic targeting.Signal transduction and targeted therapy · 2026Review
- Nicotine-Induced VEGF Levels in NSCLC Cells Are Modulated by PKA, Hyaluronan, and p53.International journal of molecular sciences · 2025Article
- HER2; p53 Co-mutated Cancers Show Increased Histone Acetylation and are Sensitive to Neratinib plus Trastuzumab Deruxtecan.bioRxiv : the preprint server for biology · 2025Article
- Myrtenol ameliorates inflammatory, oxidative, apoptotic, and hyperplasic effects of urethane-induced atypical adenomatous hyperplasia in the rat lung.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- PLK3 weakens antioxidant defense and inhibits proliferation of porcine Leydig cells under oxidative stress.Scientific reports · 2025Article
- Comprehensive analysis reveals PLK3 as a promising immune target and prognostic indicator in glioma.Oncology research · 2025Article
- p53 Genetics and Biology in Lung Carcinomas: Insights, Implications and Clinical Applications.Biomedicines · 2024Review
- Article
- PLK3 is linked with higher tumor stage and unfavorable prognosis in patients with colorectal cancer.Biomarkers in medicine · 2024Article
- High PLK3 levels are linked with less tumor invasion, lower FIGO stage and better prognosis of endometrial cancer.Biomarkers in medicine · 2024Article
- Targeting the p53 signaling pathway in cancers: Molecular mechanisms and clinical studies.MedComm · 2023Review
- The ubiquitin ligase TRIM21 regulates mutant p53 accumulation and gain of function in cancer.The Journal of clinical investigation · 2023Article
- Toward Accurate Coarse-Grained Simulations of Disordered Proteins and Their Dynamic Interactions.Journal of chemical information and modeling · 2022Article
- Article
- Mutant p53 Depletion by Novel Inhibitors for HSP40/J-Domain Proteins Derived from the Natural Compound Plumbagin.Cancers · 2022Article
- Article
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
Abstract
p53 mutations with single amino acid changes in cancer often lead to dominant oncogenic changes. Here, we have developed a mouse model of gain-of-function (GOF) p53-driven lung cancer utilizing conditionally active LSL p53-R172H and LSL K-Ras-G12D knock-in alleles that can be activated by Cre in lung club cells. Mutation of the p53 transactivation domain (TAD) (p53-L25Q/W26S/R172H) eliminating significant transactivation activity resulted in loss of tumorigenicity, demonstrating that transactivation mediated by or dependent on TAD is required for oncogenicity by GOF p53. GOF p53 TAD mutations significantly reduce phosphorylation of nearby p53 serine 20 (S20), which is a target for PLK3 phosphorylation. Knocking out PLK3 attenuated S20 phosphorylation along with transactivation and oncogenicity by GOF p53, indicating that GOF p53 exploits PLK3 to trigger its transactivation capability and exert oncogenic functions. Our data show a mechanistic involvement of PLK3 in mutant p53 pathway of oncogenesis.
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