ArticleOncogene2013
The deubiquitylase USP37 links REST to the control of p27 stability and cell proliferation.
Article in Oncogene, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 28 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.
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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
28 citing papers in PubMed, 45 citations in OpenAlex.
- Identification of Raptor and GLI1 as USP37 substrates highlight its context-specific function in medulloblastoma cells.Oncogene · 2026Article
- REST-dependent downregulation of von Hippel-Lindau tumor suppressor promotes autophagy in SHH-medulloblastoma.Scientific reports · 2024Article
- Deubiquitylating Enzymes in Cancer and Immunity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Review
- Functions of SRPK, CLK and DYRK kinases in stem cells, development, and human developmental disorders.FEBS letters · 2023Review
- Ubiquitin specific peptidase 37 and PCNA interaction promotes osteosarcoma pathogenesis by modulating replication fork progression.Journal of translational medicine · 2023Article
- Roles of the Neuron-Restrictive Silencer Factor in the Pathophysiological Process of the Central Nervous System.Frontiers in cell and developmental biology · 2022Review
- Cross-Talk Between Histone Methyltransferases and Demethylases Regulate REST Transcription During Neurogenesis.Frontiers in oncology · 2022Article
- Ubiquitin-specific peptidase 37: an important cog in the oncogenic machinery of cancerous cells.Journal of experimental & clinical cancer research : CR · 2021Review
- The Involvement of Ubiquitination Machinery in Cell Cycle Regulation and Cancer Progression.International journal of molecular sciences · 2021Review
- REST promotes ETS1-dependent vascular growth in medulloblastoma.Molecular oncology · 2021Article
- PLAGL2 promotes the proliferation and migration of gastric cancer cells via USP37-mediated deubiquitination of Snail1.Theranostics · 2021Article
- Histone deacetylase inhibitors induce medulloblastoma cell death independent of HDACs recruited in REST repression complexes.Molecular genetics & genomic medicine · 2020Article
- Critical Roles of Deubiquitinating Enzymes in the Nervous System and Neurodegenerative Disorders.Molecules and cells · 2020Review
- Preparation for DNA replication: the key to a successful S phase.FEBS letters · 2019Review
- The role of ubiquitin-specific peptidases in cancer progression.Journal of biomedical science · 2019Review
- Transcriptional repressor REST drives lineage stage-specific chromatin compaction atScience signaling · 2019Article
- Pharmacological inhibition of LSD1 activity blocks REST-dependent medulloblastoma cell migration.Cell communication and signaling : CCS · 2018Article
- Epigenetic regulation in medulloblastoma.Molecular and cellular neurosciences · 2018Review
- Article
- Regulation ofMolecular cancer research : MCR · 2017Article
Corrections and comments
- Erratum issued
Authors and funding
12 authors at 3 institutions in 1 country.
Funding
Abstract
The RE1 silencing transcription factor (REST) is a repressor of neuronal differentiation and its elevated expression in neural cells blocks neuronal differentiation. In this study, we demonstrate a role for REST in the control of proliferation of medulloblastoma cells. REST expression decreased the levels of cyclin-dependent kinase (CDK)NIB/p27, a CDK inhibitor and a brake of cell proliferation in these cells. The reciprocal relationship between REST and p27 was validated in human tumor samples. REST knockdown in medulloblastoma cells derepessed a novel REST target gene encoding the deubiquitylase ubiquitin (Ub)-specific peptidase 37 (USP37). Ectopically expressed wild-type USP37 formed a complex with p27, promoted its deubiquitination and stabilization and blocked cell proliferation. Knockdown of REST and USP37 prevented p27 stabilization and blocked the diminution in proliferative potential that normally accompanied REST loss. Unexpectedly, wild-type USP37 expression also induced the expression of REST-target neuronal differentiation genes even though REST levels were unaffected. In contrast, a mutant of USP37 carrying a site-directed change in a conserved cysteine failed to rescue REST-mediated p27 destabilization, maintenance of cell proliferation and blockade to neuronal differentiation. Consistent with these findings, a significant correlation between USP37 and p27 was observed in patient tumors. Collectively, these findings provide a novel connection between REST and the proteasomal machinery in the control of p27 and cell proliferation in medulloblastoma cells.
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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.