ReviewJournal of biomedical science2012
The role of PML ubiquitination in human malignancies.
Review in Journal of biomedical science, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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
25 citing papers in PubMed, 36 citations in OpenAlex.
- Precision post-translational modification of PML defines neuroblastoma clinical behaviour.Clinical and translational medicine · 2026Article
- Simulation and Computational Study of RING Domain Mutants of BRCA1 and Ube2k in AD/PD Pathophysiology.Molecular biotechnology · 2024Article
- CK2 and the Hallmarks of Cancer.Biomedicines · 2022Review
- Roles of ubiquitination in the crosstalk between tumors and the tumor microenvironment (Review).International journal of oncology · 2022Review
- The roles of KLHL family members in human cancers.American journal of cancer research · 2022Review
- PML-II regulates ERK and AKT signal activation and IFNα-induced cell death.Cell communication and signaling : CCS · 2021Article
- Autophagic degradation of PML promotes susceptibility to HSV-1 by stress-induced corticosterone.Theranostics · 2020Article
- Ubiquitination of tumor suppressor PML regulates prometastatic and immunosuppressive tumor microenvironment.The Journal of clinical investigation · 2017Article
- Article
- PML degradation fosters an immunosuppressive and pro-metastatic tumor microenvironment.Molecular & cellular oncology · 2017Article
- Article
- Cul3-KLHL20 ubiquitin ligase: physiological functions, stress responses, and disease implications.Cell division · 2016Review
- Cullin 3 Ubiquitin Ligases in Cancer Biology: Functions and Therapeutic Implications.Frontiers in oncology · 2016Review
- Prognostic significance of promyelocytic leukemia expression in gastrointestinal stromal tumor; integrated proteomic and transcriptomic analysis.Cancer science · 2015Article
- The function, regulation and therapeutic implications of the tumor suppressor protein, PML.Cell & bioscience · 2015Review
- Expression of neddylation-related proteins in melanoma cell lines and the effect of neddylation on melanoma proliferation.Oncology letters · 2014Article
- Topoisomerase II and leukemia.Annals of the New York Academy of Sciences · 2014Review
- USP11 regulates PML stability to control Notch-induced malignancy in brain tumours.Nature communications · 2014Article
- Activation of protein kinase CK2 attenuates FOXO3a functioning in a PML-dependent manner: implications in human prostate cancer.Cell death & disease · 2013Article
- NEDD4-1 regulates migration and invasion of glioma cells through CNrasGEF ubiquitination in vitro.PloS one · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tumor suppressors are frequently downregulated in human cancers and understanding of the mechanisms through which tumor cells restrict the expression of tumor suppressors is important for the prognosis and intervention of diseases. The promyelocytic leukemia (PML) protein plays a critical role in multiple tumor suppressive functions, such as growth inhibition, apoptosis, replicative senescence, suppression of oncogenic transformation, and inhibition of migration and angiogenesis. These tumor suppression functions are recapitulated in several mouse models. The expression of PML protein is frequently downregulated in diverse types of human tumors and this downregulation often correlates with tumor progression. Recent evidence has emerged that PML is aberrantly degraded in various types of tumors through ubiquitination-dependent mechanisms. Here, we summarize our current understanding of the PML ubiquitination/degradation pathways in human cancers. We point out that multiple pathways lead to PML ubiquitination and degradation. Furthermore, the PML ubiquitination processes are often dependent on other types of posttranslational modifications, such as phosphorylation, prolylisomerization, and sumoylation. Such feature indicates a highly regulated nature of PML ubiquitination in different cellular conditions and cell contexts, thus providing many avenues of opportunity to intervene PML ubiquitination pathways. We discuss the potential of targeting PML ubiquitination pathways for anti-cancer therapeutic strategies.
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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.