ArticlePloS one2011
High-level expression of wild-type p53 in melanoma cells is frequently associated with inactivity in p53 reporter gene assays.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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36 citing papers in PubMed, 62 citations in OpenAlex.
- In Vitro Effects of Anaesthetic Compounds on a Panel of Solid Tumour Cell Lines-An Exploratory Study.Journal of cellular and molecular medicine · 2026Article
- Regulatory roles of N6-methyladenosine methylation factors in melanoma invasion and metastasis (Review).Oncology letters · 2026Review
- Identification and characterization of BRAF⇔TP53 interactions in melanoma.Cell reports · 2026Article
- Tumor antigen PRAME promotes melanoma growth by inactivating p53 through the SIRT1-DBC1 axis.Oncogene · 2025Article
- Advances in cold atmospheric plasma therapy for cancer.Bioactive materials · 2025Review
- Tumor antigen PRAME is a potential therapeutic target of p53 activation in melanoma cells.BMB reports · 2024Article
- It is not all about the alpha: elevated expression of p53β variants is associated with lower probability of survival in a retrospective melanoma cohort.Cancer cell international · 2023Article
- Porokeratosis is one of the most common genodermatoses and is associated with an increased risk of keratinocyte cancer and melanoma.Journal of the European Academy of Dermatology and Venereology : JEADV · 2023Article
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- Tumor suppressor protein p53 expressed in yeast can remain diffuse, form a prion, or form unstable liquid-like droplets.iScience · 2021Article
- Expression levels of FBXW7 and MDM2 E3 ubiquitin ligases and their c-Myc and p53 substrates in patients with dysplastic nevi or melanoma.Oncology letters · 2021Article
- Collective cancer invasion forms an integrin-dependent radioresistant niche.The Journal of experimental medicine · 2020Article
- IFN-gamma-induced PD-L1 expression in melanoma depends on p53 expression.Journal of experimental & clinical cancer research : CR · 2019Article
- Expression profiles of p53/p73, NME and GLI families in metastatic melanoma tissue and cell lines.Scientific reports · 2019Article
- The Benefit of Reactivating p53 under MAPK Inhibition on the Efficacy of Radiotherapy in Melanoma.Cancers · 2019Article
- A meta-analysis of transcriptome datasets characterizes malignant transformation from melanocytes and nevi to melanoma.Oncology letters · 2018Article
- Scaffold Proteins in Gastrointestinal Tumors as a Shortcut to Oncoprotein Activation.Gastrointestinal tumors · 2017Review
- Unbalancing p53/Mdm2/IGF-1R axis by Mdm2 activation restrains the IGF-1-dependent invasive phenotype of skin melanoma.Oncogene · 2017Article
- p53 targets TSPAN8 to prevent invasion in melanoma cells.Oncogenesis · 2017Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundInactivation of the p53 pathway that controls cell cycle progression, apoptosis and senescence, has been proposed to occur in virtually all human tumors and p53 is the protein most frequently mutated in human cancer. However, the mutational status of p53 in melanoma is still controversial; to clarify this notion we analysed the largest series of melanoma samples reported to date. METHODOLOGY/PRINCIPAL
findingsImmunohistochemical analysis of more than 180 melanoma specimens demonstrated that high levels of p53 are expressed in the vast majority of cases. Subsequent sequencing of the p53 exons 5-8, however, revealed only in one case the presence of a mutation. Nevertheless, by means of two different p53 reporter constructs we demonstrate transcriptional inactivity of wild type p53 in 6 out of 10 melanoma cell lines; the 4 other p53 wild type melanoma cell lines exhibit p53 reporter gene activity, which can be blocked by shRNA knock down of p53. CONCLUSIONS/SIGNIFICANCE: In melanomas expressing high levels of wild type p53 this tumor suppressor is frequently inactivated at transcriptional level.
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