ArticleOncotarget2017
MYSM1/2A-DUB is an epigenetic regulator in human melanoma and contributes to tumor cell growth.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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.
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Who cites it
12 citing papers in PubMed, 20 citations in OpenAlex.
- Splicing control by PHF5A is crucial for melanoma cell survival.Cell proliferation · 2025Article
- MiR-129-5p alleviates depression and anxiety by increasing astrocyte ATP production partly through targeting deubiquitinase Mysm1.PloS one · 2025Article
- Deubiquitinase MYSM1: An Important Tissue Development and Function Regulator.International journal of molecular sciences · 2024Review
- MYSM1 acts as a novel co-activator of ERα to confer antiestrogen resistance in breast cancer.EMBO molecular medicine · 2024Article
- Genetic and Pharmacological Inhibition of Astrocytic Mysm1 Alleviates Depressive-Like Disorders by Promoting ATP Production.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- Review
- MYSM1 induces apoptosis and sensitizes TNBC cells to cisplatin via RSK3-phospho-BAD pathway.Cell death discovery · 2022Article
- Interaction of Deubiquitinase 2A-DUB/MYSM1 with DNA Repair and Replication Factors.International journal of molecular sciences · 2020Article
- Deubiquitinase MYSM1 in the Hematopoietic System and beyond: A Current Review.International journal of molecular sciences · 2020Review
- Article
- Targeted Tumor Therapy Remixed-An Update on the Use of Small-Molecule Drugs in Combination Therapies.Cancers · 2018Review
- 2A-DUB/Mysm1 Regulates Epidermal Development in Part by Suppressing p53-Mediated Programs.International journal of molecular sciences · 2018Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Histone modifying enzymes, such as histone deacetylases (HDACs) and polycomb repressive complex (PRC) components, have been implicated in regulating tumor growth, epithelial-mesenchymal transition, tumor stem cell maintenance, or repression of tumor suppressor genes - and may be promising targets for combination therapies of melanoma and other cancers. According to recent findings, the histone H2A deubiquitinase 2A-DUB/Mysm1 interacts with the p53-axis in hematopoiesis and tissue differentiation in mice, in part by modulating DNA-damage responses in stem cell and progenitor compartments. Based on the identification of alterations in skin pigmentation and melanocyte specification in Mysm1-deficient mice, we hypothesized that MYSM1 may be involved in melanoma formation. In human melanoma samples, expression of MYSM1 was increased compared with normal skin melanocytes and nevi and co-localized with melanocyte markers such as Melan-A and c-KIT. Similarly, in melanoma cell lines A375 and SK-MEL-28 and in murine skin, expression of the deubiquitinase was detectable at the mRNA and protein level that was inducible by growth factor signals and UVB exposure, respectively. Upon stable silencing of
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