ArticleJournal of experimental & clinical cancer research : CR2023
Deubiquitylase YOD1 regulates CDK1 stability and drives triple-negative breast cancer tumorigenesis.
Article in Journal of experimental & clinical cancer research : CR, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 46 citations in OpenAlex.
- Deubiquitinase YOD1 Inhibition Suppresses DEX- and Denervation-Induced Muscle Atrophy Through MAFbx Destabilization.Journal of cachexia, sarcopenia and muscle · 2026Article
- BIRC6 prevents GSDME-mediated pyroptosis and promotes cisplatin resistance via a non-canonical UBC domain-dependent steric hindrance.Cell communication and signaling : CCS · 2026Article
- Targeting the OTU family: a core therapeutic strategy for reshaping the immunosuppressive microenvironment and reversing drug resistance in HCC by coordinating the autophagy-ferroptosis balance.Cell death discovery · 2026Review
- Deciphering the Effect of Methyl 4‑Hydroxybenzoate on Breast Cancer by Bioinformatics and Experiments.ACS omega · 2026Article
- <p>CDK1 depletion suppresses glioma malignancy through cell cycle pathway regulation: Mechanistic insights from functional and molecular profiling</p>.Oncology reports · 2026Article
- OTUD4 deubiquitination stabilizes EGFR and activates the PI3K/AKT pathway to promote the invasiveness of triple-negative breast cancer.Cell death & disease · 2026Article
- Therapeutic targeting of YOD1 disrupts the PAX-FOXO1/N-Myc feedback loop in rhabdomyosarcoma.JCI insight · 2026Article
- An integrated study combining network toxicology machine learning and molecular simulation reveals the molecular mechanisms of permanent hair dyes in breast cancer.Discover oncology · 2026Article
- OTU deubiquitinases as immune-circuit editors: from human immunopathology to therapeutic prioritization.Frontiers in immunology · 2026Review
- Machine learning-based identification of hub genes and prognostic biomarkers in prostate cancer.Frontiers in genetics · 2026Article
- Article
- OTU deubiquitinases in disease: roles and targeting.Trends in molecular medicine · 2026Review
- YOD1 promotes ferroptosis in acute lung injury by deubiquitination of NCOA4.Communications biology · 2025Article
- YOD1 mediates isoproterenol-induced cardiac remodeling by deubiquitinating PKM2 and reducing PKM2 tetramerization in cardiomyocytes.Acta pharmacologica Sinica · 2025Article
- LncRNA SOX21-AS1 Promotes the Progression of Pancreatic Cancer by Sponging miR-9-3p and Upregulating YOD1.The Kaohsiung journal of medical sciences · 2025Article
- Controlling gene expression through five zinc finger domains of ZNF18.Protein science : a publication of the Protein Society · 2025Article
- Cardiomyocyte-derived YOD1 promotes pathological cardiac hypertrophy by deubiquitinating and stabilizing STAT3.Science advances · 2025Article
- Regulation of disease signaling by YOD1: potential implications for therapeutic strategies.Cancer cell international · 2025Review
- The deubiquitinase YOD1 suppresses tumor progression by stabilizing ZNF24 in clear cell renal carcinoma.Cell death & disease · 2025Article
- Visualization analysis of breast cancer-related ubiquitination modifications over the past two decades.Discover oncology · 2025Article
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Authors and funding
16 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundAccumulating evidence has demonstrated that aberrant expression of deubiquitinating enzymes is associated with the initiation and progression of Triple-negative breast cancer (TNBC). The publicly available TCGA database of breast cancer data was used to analyze the OTUD deubiquitinating family members that were correlated with survival of breast cancer and ovarian tumor domain-containing 2 (OTUD-2), or YOD1 was identified. The aim of present study was to assess YOD1 expression and function in human TNBC and then explored the underlying molecular events.
methodsWe detected the expression of YOD1 in 32 TNBC and 44 NTNBC samples by qRT-PCR, Western blot and immunohistochemistry. Manipulation of YOD1 expression was assessed in vitro and in vivo for TNBC cell proliferation, migration, invasion, cell-cycle and drug resistance, using colony formation assay, transwell assay, CCK8 assay, TUNEL assay, flow cytometric analysis and xenograft tumor assay. Next, proteomic analysis, Western blot, proximity ligation assay, Immunoprecipitation, and Immunofluorescence were conducted to assess downstream targets.
resultsIt was found that YOD1 was significantly upregulated in TNBC tissues compared with non-triple-negative breast cancer (NTNBC), which was positively correlated with poor survival in TNBC patients. Knockdown of YOD1 effectively inhibited TNBC cell migration, proliferation, cell cycle and resistance to cisplatin and paclitaxel. Mechanistically, YOD1 promoted TNBC progression in a manner dependent on its catalytic activity through binding with CDK1, leading to de-polyubiquitylation of CDK1 and upregulation of CDK1 expression. In addition, YOD1 overexpression was found to be correlated with CDK1 overexpression in human TNBC specimens. Finally, in vivo study demonstrated that YOD1 knockdown or YOD1 inhibitor could inhibit CDK1 expression and suppress the growth and metastasis of TNBC tumors.
conclusionOur study highlights that YOD1 functions as an oncogene in TNBC via binding to CDK1 and mediated its stability and oncogenic activity. Interfering with YOD1 expression or YOD1 inhibitor could suppress TNBC cells in vitro and in vivo, suggesting that YOD1 may prove to be a promising therapeutic target for TNBC.
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