ArticleProceedings of the National Academy of Sciences of the United States of America2014
Pla2g16 phospholipase mediates gain-of-function activities of mutant p53.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.
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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.
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Who cites it
66 citing papers in PubMed, 101 citations in OpenAlex.
- Multiple ETS family transcription factors bind mutant p53 via distinct interaction regions.FEBS letters · 2026Article
- Multiple roles of p53 in cancer development: Regulation of tumor microenvironment, mJournal of advanced research · 2025Review
- PLA2G16 expression predicts prognosis and gemcitabine sensitivity in patients with pancreatic cancer.PeerJ · 2025Article
- Receptors and Host Factors for Enterovirus Infection: Implications for Cancer Therapy.Cancers · 2024Review
- p53R172H and p53R245W Hotspot Mutations Drive Distinct Transcriptomes in Mouse Mammary Tumors Through a Convergent Transcriptional Mediator.Cancer research communications · 2024Article
- Cell fate regulation governed by p53: Friends or reversible foes in cancer therapy.Cancer communications (London, England) · 2024Review
- Metabolism-regulating non-coding RNAs in breast cancer: roles, mechanisms and clinical applications.Journal of biomedical science · 2024Review
- Mutant p53 protects triple-negative breast adenocarcinomas from ferroptosis in vivo.Science advances · 2024Article
- p53R245W Mutation Fuels Cancer Initiation and Metastases in NASH-driven Liver Tumorigenesis.Cancer research communications · 2023Article
- Triple-negative breast tumors are dependent on mutant p53 for growth and survival.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Unique Transcriptional Profiles Underlie Osteosarcomagenesis Driven by Different p53 Mutants.Cancer research · 2023Article
- Cuproptosis: p53-regulated metabolic cell death?Cell death and differentiation · 2023Review
- The complexity of p53-mediated metabolic regulation in tumor suppression.Seminars in cancer biology · 2022Review
- Disruption of tp53 leads to cutaneous nevus and melanoma formation in Xenopus tropicalis.Molecular oncology · 2022Article
- Differential Gain-of-Function Activity of Three p53 Hotspot Mutants In Vivo.Cancer research · 2022Article
- Current Knowledge on Mammalian Phospholipase AMolecules (Basel, Switzerland) · 2022Review
- A novel lncRNA ROPM-mediated lipid metabolism governs breast cancer stem cell properties.Journal of hematology & oncology · 2021Article
- Targeting mutant p53 for cancer therapy: direct and indirect strategies.Journal of hematology & oncology · 2021Review
- TP53 in Biology and Treatment of Osteosarcoma.Cancers · 2021Review
- OncogenicCancer discovery · 2021Article
6 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
21 authors at 5 institutions in 2 countries.
Funding
Abstract
p53(R172H/+) mice inherit a p53 mutation found in Li-Fraumeni syndrome and develop metastatic tumors at much higher frequency than p53(+/-) mice. To explore the mutant p53 metastatic phenotype, we used expression arrays to compare primary osteosarcomas from p53(R172H/+) mice with metastasis to osteosarcomas from p53(+/-) mice lacking metastasis. For this study, 213 genes were differentially expressed with a P value <0.05. Of particular interest, Pla2g16, which encodes a phospholipase that catalyzes phosphatidic acid into lysophosphatidic acid and free fatty acid (both implicated in metastasis), was increased in p53(R172H/+) osteosarcomas. Functional analyses showed that Pla2g16 knockdown decreased migration and invasion in mutant p53-expressing cells, and vice versa: overexpression of Pla2g16 increased the invasion of p53-null cells. Furthermore, Pla2g16 levels were increased upon expression of mutant p53 in both mouse and human osteosarcoma cell lines, indicating that Pla2g16 is a downstream target of the mutant p53 protein. ChIP analysis revealed that several mutant p53 proteins bind the Pla2g16 promoter at E26 transformation-specific (ETS) binding motifs and knockdown of ETS2 suppressed mutant p53 induction of Pla2g16. Thus, our study identifies a phospholipase as a transcriptional target of mutant p53 that is required for metastasis.
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Registered trials
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