ArticleNature communications2016
COPS5 amplification and overexpression confers tamoxifen-resistance in ERα-positive breast cancer by degradation of NCoR.
Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 2 of them syntheses that pooled it.
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Who cites it
34 citing papers in PubMed, 2 syntheses or guidelines pooled it, 75 citations in OpenAlex.
- Prognostic value of CSN5 in patients with digestive system cancers: a systematic review and meta-analysis.BMC cancer · 2022Pooled it
- Prognostic role of c-Jun activation domain-binding protein-1 in cancer: A systematic review and meta-analysis.Journal of cellular and molecular medicine · 2021Pooled it
- JAB1/CRL4B complex represses PPARG/ACSL5 expression to promote breast tumorigenesis.Cell death and differentiation · 2026Article
- Jab1 promotes immune evasion and progression in acute myeloid leukemia models under oxidative stress.The Journal of clinical investigation · 2025Article
- COPS5 Triggers Ferroptosis Defense by Stabilizing MK2 in Hepatocellular Carcinoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- A novel CSN5/CRT O-GlcNAc/ER stress regulatory axis in platinum resistance of epithelial ovarian cancer.International journal of biological sciences · 2024Article
- Landscape of NcRNAs involved in drug resistance of breast cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023Review
- Regulatory mechanisms and therapeutic potential of JAB1 in neurological development and disorders.Molecular medicine (Cambridge, Mass.) · 2023Review
- COPS5 Conferred the Platinum Resistance in Epithelial Ovarian Cancer.Current issues in molecular biology · 2022Article
- Prognostic and therapeutic significance of COP9 signalosome subunit CSN5 in prostate cancer.Oncogene · 2022Article
- Endocrine resistance in breast cancer: from molecular mechanisms to therapeutic strategies.Journal of molecular medicine (Berlin, Germany) · 2021Review
- Jab1/Cops5: a promising target for cancer diagnosis and therapy.International journal of clinical oncology · 2021Review
- TNFα Enhances Tamoxifen Sensitivity through Dissociation of ERα-p53-NCOR1 Complexes in ERα-Positive Breast Cancer.Cancers · 2021Article
- Overcoming oncogene addiction in breast and prostate cancers: a comparative mechanistic overview.Endocrine-related cancer · 2021Review
- Identification of Key Transcription Factors and Immune Infiltration Patterns Associated With Breast Cancer Prognosis Using WGCNA and Cox Regression Analysis.Frontiers in oncology · 2021Article
- The transcription co-factor JAB1/COPS5, serves as a potential oncogenic hub of human chondrosarcoma cellsAmerican journal of cancer research · 2021Article
- Identification of MMP1 as a potential gene conferring erlotinib resistance in non-small cell lung cancer based on bioinformatics analyses.Hereditas · 2020Article
- Article
- Overcoming Endocrine Resistance in Breast Cancer.Cancer cell · 2020Review
- Inhibition of USP14 Deubiquitinating Activity as a Potential Therapy for Tumors withMolecular therapy oncolytics · 2020Article
Corrections and comments
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Authors and funding
12 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oestrogen receptor α (ERα) antagonists are used in endocrine therapies for ERα-positive (ERα+) breast cancer patients. Unfortunately the clinical benefit is limited due to intrinsic and acquired drug resistance. Here using integrated genomic and functional studies, we report that amplification and/or overexpression of COPS5 (CSN5/JAB1) confers resistance to tamoxifen. Amplification and overexpression of COPS5, a catalytic subunit of the COP9 complex, is present in about 9% of the ERα+ primary breast cancer and more frequently (86.7%, 26/30) in tamoxifen-refractory tumours. Overexpression of COPS5, through its isopeptidase activity, leads to ubiquitination and proteasome-mediated degradation of NCoR, a key corepressor for ERα and tamoxifen-mediated suppression of ERα target genes. Importantly, COPS5 overexpression causes tamoxifen-resistance in preclinical breast cancer models in vitro and in vivo. We also demonstrate that genetic inhibition of the isopeptidase activity of COPS5 is sufficient to re-sensitize the resistant breast cancer cells to tamoxifen-treatment, offering a potential therapeutic approach for endocrine-resistant breast cancer patients.
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