ArticleThe EMBO journal2008
p73 poses a barrier to malignant transformation by limiting anchorage-independent growth.
Article in The EMBO journal, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
25 citing papers in PubMed, 49 citations in OpenAlex.
- The construction of a novel prognostic prediction model for glioma based on GWAS-identified prognostic-related risk loci.Open medicine (Warsaw, Poland) · 2024Article
- Grading of lung adenocarcinomas with simultaneous segmentation by artificial intelligence (GLASS-AI).NPJ precision oncology · 2023Article
- Review
- CBFB cooperates with p53 to maintain TAp73 expression and suppress breast cancer.PLoS genetics · 2021Article
- Loss of stretch-activated channels, PIEZOs, accelerates non-small cell lung cancer progression and cell migration.Bioscience reports · 2019Article
- Article
- Article
- A balancing act: orchestrating amino-truncated and full-length p73 variants as decisive factors in cancer progression.Oncogene · 2015Review
- The family of K2P channels: salient structural and functional properties.The Journal of physiology · 2015Review
- ∆Np73 is capable of inducing apoptosis by co-ordinately activating several BH3-only proteins.Bioscience reports · 2015Article
- TAp73 suppresses tumor angiogenesis through repression of proangiogenic cytokines and HIF-1α activity.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Piezo channels: from structure to function.Pflugers Archiv : European journal of physiology · 2015Review
- Monitoring the dynamics of clonal tumour evolution in vivo using secreted luciferases.Nature communications · 2014Article
- Nuclear receptor CAR specifically activates the two-pore K+ channel Kcnk1 gene in male mouse livers, which attenuates phenobarbital-induced hepatic hyperplasia.Toxicological sciences : an official journal of the Society of Toxicology · 2013Article
- p53 Family: Role of Protein Isoforms in Human Cancer.Journal of nucleic acids · 2012Article
- Oncogenic functions of hMDMX in in vitro transformation of primary human fibroblasts and embryonic retinoblasts.Molecular cancer · 2011Article
- p73 in Cancer.Genes & cancer · 2011Article
- p73 as a pharmaceutical target for cancer therapy.Current pharmaceutical design · 2011Review
- Analysis of the intracellular localization of p73 N-terminal protein isoforms TAp73 and ∆Np73 in medulloblastoma cell lines.Journal of molecular histology · 2010Article
- Malignant transformation in a defined genetic background: proteome changes displayed by 2D-PAGE.Molecular cancer · 2010Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
p53 is known to prevent tumour formation by restricting the proliferation of damaged or oncogene-expressing cells. In contrast, how the p53 family member p73 suppresses tumour formation remains elusive. Using a step-wise transformation protocol for human cells, we show that, in premalignant stages, expression of the transactivation-competent p73 isoform TAp73 is triggered in response to pRB pathway alterations. TAp73 expression at this stage of transformation results in increased sensitivity to chemotherapeutic drugs and oxidative stress and inhibits proliferation and survival at high cell density. Importantly, TAp73 triggers a transcriptional programme to prevent anchorage-independent growth, which is considered a crucial hallmark of fully transformed cells. An essential suppressor of anchorage-independent growth is KCNK1, which is directly transactivated by TAp73 and commonly downregulated in glioma, melanoma and ovarian cancer. Oncogenic Ras switches p73 expression from TAp73 to the oncogenic deltaNp73 isoform in a phosphatidyl-inositol 3-kinase-dependent manner. Our results implicate TAp73 as a barrier to anchorage-independent growth and indicate that downregulation of TAp73 is a key transforming activity of oncogenic Ras 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.