ArticleTranslational lung cancer research2021
Deubiquitinase USP5 promotes non-small cell lung cancer cell proliferation by stabilizing cyclin D1.
Article in Translational lung cancer research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 56 citations in OpenAlex.
- USP5 in cancer: a therapeutic window into metabolism and drug resistance.Journal of translational medicine · 2026Review
- Expression, regulation, and multifaceted molecular and biological functions of sirtuin 6 in the porcine endometrium during early pregnancy.Cell communication and signaling : CCS · 2026Article
- Ubiquitination and deubiquitination as critical modulators of NSCLC tumorigenesis and drug resistance.Discover oncology · 2026Review
- Molecular regulation by ubiquitin-specific proteases (USPs) in HCC: cell cycle, oncogenic signaling, and beyond.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Establishment and characterization of an orthotopic implanted lung cancer model to mimic human tumor structure, microenvironment, and metastatic spread.Translational lung cancer research · 2025Article
- EOAI3402143 inhibits lung adenocarcinoma progression through the NF-κB/NR4A1 pathway.Acta biochimica et biophysica Sinica · 2025Article
- Regulatory Functions of microRNAs in Cancer Stem Cells: Mechanism, Facts, and Perspectives.Cells · 2025Review
- Mechanistic Insights and Therapeutic Potentials of Ubiquitin-Proteasome System in Non-Small Cell Lung Cancer.Cell proliferation · 2025Review
- SP1 promotes triple-negative breast cancer progression by targeting USP5.Cancer cell international · 2025Article
- Deubiquitinase USP18 mediates cell migration, apoptosis and ferroptosis in lung adenocarcinoma by depending on POU4F1/PRKAA2 axis.BMC cancer · 2025Article
- Ubiquitin-Specific Protease Inhibitors for Cancer Therapy: Recent Advances and Future Prospects.Biomolecules · 2025Review
- Chemical tools to define and manipulate interferon-inducible Ubl protease USP18.Nature communications · 2025Article
- USP5 promotes tumor progression by stabilizing SLUG in bladder cancer.Oncology letters · 2024Article
- USP5 Promotes Ripretinib Resistance in Gastrointestinal Stromal Tumors by MDH2 Deubiquition.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Unraveling the Immune Regulatory Functions of USP5: Implications for Disease Therapy.Biomolecules · 2024Review
- Regulatory role of the miR-142-3p/Translational lung cancer research · 2024Article
- BRD7 enhances the radiosensitivity of nasopharyngeal carcinoma cells by negatively regulating USP5/METTL3 axis-mediated homologous recombination repair.International journal of biological sciences · 2024Article
- Unraveling the Mechanism of Action of Ubiquitin-Specific Protease 5 and Its Inhibitors in Tumors.Clinical Medicine Insights. Oncology · 2024Review
- Hsa_circ_0102899 promotes epithelial-mesenchymal transition in non-small cell lung cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023Article
- Targeting the deubiquitinaseOncology reports · 2023Review
Corrections and comments
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Authors and funding
14 authors at 6 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCyclin D1 (CCND1) is overexpressed in non-small cell lung cancer (NSCLC) and contributes to its tumorigenesis and progression. Accumulating evidence shows that ubiquitin-specific protease 5 (USP5), an important member of the USP family, acts as a tumor promoter by deubiquitinating and stabilizing oncoproteins. However, neither the mechanism for dysregulated turnover of CCND1 protein nor the association of CCND1 with USP5 in NSCLC is well understood.
methodsThe association of USP5 with CCND1 in human NSCLC cells and clinical tissues was determined by immunoprecipitation/immunoblotting, immunohistochemistry (IHC), and The Cancer Genome Atlas database analyses. The effect of USP5 knockdown or overexpression on NSCLC cell proliferation
resultsUSP5 physically bound to CCND1 and decreased its polyubiquitination level, thereby stabilizing CCND1 protein. This USP5-CCND1 axis promoted NSCLC cell proliferation and colony formation. Further, knockdown of USP5 led to CCND1 degradation and cell cycle arrest in NSCLC cells. Importantly, this tumor-suppressive effect elicited by USP5 knockdown in NSCLC cells was validated
conclusionsThis study has provided the first evidence that CCND1 is a novel substrate of USP5. The USP5-CCND1 axis could be a potential target for the treatment of NSCLC.
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