ArticleJournal of cancer research and clinical oncology2021
p53 is functionally inhibited in clear cell renal cell carcinoma (ccRCC): a mechanistic and correlative investigation into genetic and molecular characteristics.
Article in Journal of cancer research and clinical oncology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 12 citations in OpenAlex.
- A single chromosome 3p break initiates clear cell renal cell carcinoma evolution.bioRxiv : the preprint server for biology · 2026Article
- The p53 Isoforms as Potential Biomarkers in Different Cancer Entities.International journal of molecular sciences · 2026Review
- Dual loss of VHL and RASSF1A enhances tumorigenicity in clear cell renal cancer.Frontiers in oncology · 2026Article
- MAOB promotes ROS-mediated DNA damage, triggering a cyclic MAOB-HNF1A-53BP1-p53 axis that suppresses the malignancy of clear cell renal cell carcinoma.Redox biology · 2025Article
- PUMA reduces FASN ubiquitination to promote lipid accumulation and tumor progression in human clear cell renal cell carcinoma.Cell death & disease · 2025Article
- The molecular mechanism of NF-κB dysregulation across different subtypes of renal cell carcinoma.Journal of advanced research · 2025Review
- USP7 depletion potentiates HIF2α degradation and inhibits clear cell renal cell carcinoma progression.Cell death & disease · 2024Article
- The establishment of kidney cancer organoid line in drug testing.Cancer medicine · 2024Article
- Article
- Review
- Review
- p53 and Its Isoforms in Renal Cell Carcinoma-Do They Matter?Biomedicines · 2022Review
Corrections and comments
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Authors and funding
15 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeAlthough p53 is rarely mutated in ccRCC, its overexpression has been linked to poor prognosis. The current study sought to elucidate the unique role of p53 in ccRCC with genomic, proteomic, and functional analyses. MATERIALS AND
methodsData from the Cancer Genome Atlas (TCGA) were evaluated for genomic and proteomic characteristics of p53; a tissue micro array (TMA) study was carried out to evaluate the association of p53 and phosphorylated p53 (pp53) with clinical outcome. Mechanistic in vitro experiments were performed to confirm a pro-apoptotic loss of p53 in ccRCC and p53 isoforms as well as posttranslational modifications of p53 where assessed to provide possible reasons for a functional inhibition of p53 in ccRCC.
resultsA low somatic mutation rate of p53 could be confirmed. Although mRNA levels were correlated with poor prognosis and clinicopathological features, there was no monotonous association of mRNA levels with survival outcome. Higher p53 protein levels could be confirmed as poor prognostic features. In vitro, irradiation of ccRCC cell lines markedly induced levels of p53 and of activated (phosphorylated) p53. However, irradiated ccRCC cells demonstrated similar proliferation, migration, and p53 transcriptional activity like non-irradiated controls indicating a functional inhibition of p53. p53 isoforms and could not be correlated with clinical outcome of ccRCC patients.
conclusionsp53 is rarely mutated but the wildtype p53 is functionally inhibited in ccRCC. To investigate mechanisms that underlie functional inhibition of p53 may provide attractive therapeutic targets in ccRCC.
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