ReviewFrontiers in cell and developmental biology2022
It's Getting Complicated-A Fresh Look at p53-MDM2-ARF Triangle in Tumorigenesis and Cancer Therapy.
Review in Frontiers in cell and developmental biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 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.
The trial behind it
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
41 citing papers in PubMed, 60 citations in OpenAlex.
- Opportunities in cancer gene therapy: inhibiting MDM2 and restoring p14ARF as a means to activate p53.Molecular and cellular biochemistry · 2026Review
- A high-density CRISPR activation platform for mapping cancer dependencies and resistance pathways ex vivo and in vivo.Science advances · 2026Article
- Reversible Nucleolar Stress and Cell Growth Arrest Triggered by Acidic pH.Journal of cellular physiology · 2026Article
- The Interaction of Structural Analogues of Phenothiazines in p53-Dependent Cellular Signaling Pathways.ACS omega · 2026Article
- Nucleolus as a cornerstone linking proliferation and metabolism to cellular responses to stress: involvement of transcription factors MYC and p53.Frontiers in molecular biosciences · 2026Review
- Rewired DDR-TGF-β-β-catenin-PD-L1 axis accelerates progression and shapes therapy in human papillomavirus-driven cancer.Frontiers in immunology · 2026Review
- MDM2 in Tumor Biology and Cancer Therapy: A Review of Current Clinical Trials.International journal of molecular sciences · 2025Review
- Depletion of tryptophanyl-tRNA synthetase and tryptophan accumulation triggers p53-dependent apoptosis.Cell death discovery · 2025Article
- Targeting MDM2 homodimer and heterodimer disruption with DRx-098D inMolecular therapy. Oncology · 2025Article
- Diagnosis, Treatment, and Unmet Needs of Dedifferentiated Liposarcoma in the United States: A Multidisciplinary Delphi Study.Cancers · 2025Article
- The Interaction of DMRTA2 with HSP90β Inhibits p53 Ubiquitination and Activates the p53 Pathway to Suppress the Malignant Progression of Non-Small-Cell Lung Cancer.Current issues in molecular biology · 2025Article
- Limited cell-autonomous anticancer mechanisms in long-lived bats.Nature communications · 2025Article
- Expression of PSMD2 gene in hepatocellular carcinoma and its correlation with immune checkpoints and prognosis.Scientific reports · 2025Article
- Canonical and noncanonical NOTCH signaling in the nongenetic resistance of cancer: distinct and concerted control.Frontiers of medicine · 2025Review
- Exploring TGF-β Signaling in Cancer Progression: Prospects and Therapeutic Strategies.OncoTargets and therapy · 2025Review
- Unraveling Glioblastoma: TME Implication and Gene Therapy Advances.Current gene therapy · 2025Review
- p53: A player in the tumor microenvironment.Oncology research · 2025Review
- Antioxidant activity, antibacterial behavior, and anticancer impact of Egyptian propolis.Open veterinary journal · 2025Review
- Oncogenic Functions of Alternatively SplicedInternational journal of molecular sciences · 2024Article
- ARF alters PAF1 complex integrity to selectively repress oncogenic transcription programs upon p53 loss.Molecular cell · 2024Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Anti-tumorigenic mechanisms mediated by the tumor suppressor p53, upon oncogenic stresses, are our bodies' greatest weapons to battle against cancer onset and development. Consequently, factors that possess significant p53-regulating activities have been subjects of serious interest from the cancer research community. Among them, MDM2 and ARF are considered the most influential p53 regulators due to their abilities to inhibit and activate p53 functions, respectively. MDM2 inhibits p53 by promoting ubiquitination and proteasome-mediated degradation of p53, while ARF activates p53 by physically interacting with MDM2 to block its access to p53. This conventional understanding of p53-MDM2-ARF functional triangle have guided the direction of p53 research, as well as the development of p53-based therapeutic strategies for the last 30 years. Our increasing knowledge of this triangle during this time, especially through identification of p53-independent functions of MDM2 and ARF, have uncovered many under-appreciated molecular mechanisms connecting these three proteins. Through recognizing both antagonizing and synergizing relationships among them, our consideration for harnessing these relationships to develop effective cancer therapies needs an update accordingly. In this review, we will re-visit the conventional wisdom regarding p53-MDM2-ARF tumor-regulating mechanisms, highlight impactful studies contributing to the modern look of their relationships, and summarize ongoing efforts to target this pathway for effective cancer treatments. A refreshed appreciation of p53-MDM2-ARF network can bring innovative approaches to develop new generations of genetically-informed and clinically-effective cancer therapies.
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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 Socratic graph.