ArticleEMBO molecular medicine2020
Maintaining protein stability of ∆Np63 via USP28 is required by squamous cancer cells.
Article in EMBO molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 66 citations in OpenAlex.
- Targeting ubiquitin signaling vulnerabilities in KEAP1-inactivated lung cancer.The EMBO journal · 2026Article
- The dual fate of DYRK2 in cancer: balancing the light and dark side of tumorigenesis.Cancer metastasis reviews · 2026Review
- Pathological role of deubiquitinating enzymes in lung cancer: recent insights and advances.American journal of cancer research · 2026Review
- Targeting the deubiquitinase USP28 in cancer: navigating context-dependent mechanisms and therapeutic resistance.Frontiers in immunology · 2026Review
- Cancer-associated USP28 missense mutations disrupt 53BP1 interaction and p53 stabilization.Nature communications · 2025Article
- Ferroptosis and non-coding RNAs in lung cancer: exploring molecular mechanisms and diagnostic/therapeutic implications.Cancer cell international · 2025Review
- Decoding the ubiquitin network: molecular mechanisms and therapeutic vulnerabilities for precision radio-sensitization in cancer.Molecular cancer · 2025Review
- Pharmacologic interrogation of USP28 cellular function in p53 signaling.Cell chemical biology · 2025Article
- Article
- USP28 promotes PARP inhibitor resistance by enhancing SOX9-mediated DNA damage repair in ovarian cancer.Cell death & disease · 2025Article
- The deubiquitinase USP28 maintains the expression of PPARγ and its inactivation protects mice from diet-induced MASH and hepatocarcinoma.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- USP39 at the crossroads of cancer immunity: regulating immune evasion and immunotherapy response through RNA splicing and ubiquitin signaling.Frontiers in immunology · 2025Review
- Structural basis for the bi-specificity of USP25 and USP28 inhibitors.EMBO reports · 2024Article
- Hypoxia-activated XBP1s recruits HDAC2-EZH2 to engage epigenetic suppression of ΔNp63α expression and promote breast cancer metastasis independent of HIF1α.Cell death and differentiation · 2024Article
- USP13 drives lung squamous cell carcinoma by switching lung club cell lineage plasticity.Molecular cancer · 2023Article
- Deubiquitinases in cancer.Nature reviews. Cancer · 2023Review
- DARPins detect the formation of hetero-tetramers of p63 and p73 in epithelial tissues and in squamous cell carcinoma.Cell death & disease · 2023Article
- Role of c-Myc in lung cancer: Progress, challenges, and prospects.Chinese medical journal pulmonary and critical care medicine · 2023Article
- USP28 controls SREBP2 and the mevalonate pathway to drive tumour growth in squamous cancer.Cell death and differentiation · 2023Article
- The deubiquitinase USP28 maintains the expression of the transcription factor MYCN and is essential in neuroblastoma cells.The Journal of biological chemistry · 2023Article
Corrections and comments
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Authors and funding
16 authors at 4 institutions in 3 countries.
Funding
Abstract
The transcription factor ∆Np63 is a master regulator of epithelial cell identity and essential for the survival of squamous cell carcinoma (SCC) of lung, head and neck, oesophagus, cervix and skin. Here, we report that the deubiquitylase USP28 stabilizes ∆Np63 and maintains elevated ∆NP63 levels in SCC by counteracting its proteasome-mediated degradation. Impaired USP28 activity, either genetically or pharmacologically, abrogates the transcriptional identity and suppresses growth and survival of human SCC cells. CRISPR/Cas9-engineered in vivo mouse models establish that endogenous USP28 is strictly required for both induction and maintenance of lung SCC. Our data strongly suggest that targeting ∆Np63 abundance via inhibition of USP28 is a promising strategy for the treatment of SCC tumours.
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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.