ReviewCurrent pharmaceutical design2013
Targeting the ubiquitin-mediated proteasome degradation of p53 for cancer therapy.
Review in Current pharmaceutical design, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.
What it found
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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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
32 citing papers in PubMed, 1 synthesis or guideline pooled it, 58 citations in OpenAlex.
- The proteasome as a druggable target with multiple therapeutic potentialities: Cutting and non-cutting edges.Pharmacology & therapeutics · 2020Pooled it
- In silico identification of prospective p53-MDM2 inhibitors from ASINEX database using a comprehensive molecular modelling approach.Scientific reports · 2025Article
- Targeting the Ubiquitin-Proteasome System for Cancer.MedComm · 2025Review
- ATF6 supports lysosomal function in tumor cells to enable ER stress-activated macroautophagy and CMA: impact on mutant TP53 expression.Autophagy · 2024Article
- Post-Translational Modifications (PTMs) of mutp53 and Epigenetic Changes Induced by mutp53.Biology · 2024Review
- The SUMOylation and ubiquitination crosstalk in cancer.Journal of cancer research and clinical oncology · 2023Review
- HDAC11 mediates the ubiquitin-dependent degradation of p53 and inhibits the anti-leukemia effect of PD0166285.Medical oncology (Northwood, London, England) · 2023Article
- MDM2 Inhibition in the Treatment of Glioblastoma: From Concept to Clinical Investigation.Biomedicines · 2023Review
- The crosstalk between ubiquitin-conjugating enzyme E2Q1 and p53 in colorectal cancer: An in vitro analysis.Medical oncology (Northwood, London, England) · 2023Article
- Physiological Overview of the Potential Link between the UPS and CaAntioxidants (Basel, Switzerland) · 2022Review
- BRD7 Stabilizes P53 via Dephosphorylation of MDM2 to Inhibit Tumor Growth in Breast Cancer Harboring Wild-type P53.Journal of Cancer · 2022Article
- ER stress-induced modulation of neural activity and seizure susceptibility is impaired in a fragile X syndrome mouse model.Neurobiology of disease · 2021Article
- Dysregulation of the Ubiquitin Proteasome System in Human Malignancies: A Window for Therapeutic Intervention.Cancers · 2021Review
- The SUMO-specific protease SENP1 deSUMOylates p53 and regulates its activity.Journal of cellular biochemistry · 2021Article
- More Than Just Cleaning: Ubiquitin-Mediated Proteolysis in Fungal Pathogenesis.Frontiers in cellular and infection microbiology · 2021Review
- The Effect of Dysfunctional Ubiquitin Enzymes in the Pathogenesis of Most Common Diseases.International journal of molecular sciences · 2020Review
- IU1 suppresses proliferation of cervical cancer cells through MDM2 degradation.International journal of biological sciences · 2020Article
- De novo macrocyclic peptides that specifically modulate Lys48-linked ubiquitin chains.Nature chemistry · 2019Article
- PPPDE1 promotes hepatocellular carcinoma development by negatively regulate p53 and apoptosis.Apoptosis : an international journal on programmed cell death · 2019Article
- Targeting energy metabolism to eliminate cancer cells.Cancer management and research · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Within the past decade, there has been a revolution in the types of drugs developed to treat cancer. Therapies that selectively target cancer-specific aberrations, such as kinase inhibitors, have made a dramatic impact on a subset of patients. In spite of these successes, there is still a dearth of treatment options for the vast majority of patients. Therefore, there is a need to design therapies with broader efficacy. The p53 tumor suppressor pathway is one of the most frequently altered in human cancers. However, about half of all cancers retain wild-type p53, yet through various mechanisms, the p53 pathway is otherwise inactivated. Targeting this pathway for reactivation truly represents the "holy grail" in cancer treatment. Most commonly, destabilization of p53 by various components of ubiquitin- proteasome system, notably the ubiquitin ligase MDM2 and its partner MDMX as well as various deubiquitinating enzymes (DUBs), render p53 inert and unresponsive to stress signals. Reinstating its function in cancer has been a long sought-after goal. Towards this end, a great deal of work has been devoted to the development of compounds that either interfere with the p53-MDM2 and p53- MDMX interactions, inhibit MDM2 E3 activity, or target individual DUBs. Here we review the current progress that has been made in the field, with a special emphasis on both MDM2 and DUB inhibitors. Developing inhibitors targeting the upstream of the p53 ubiquitination pathway will likely also be a valuable option.
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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.