ArticleCancer research2014
USP22 regulates oncogenic signaling pathways to drive lethal cancer progression.
Article in Cancer research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 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.
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Who cites it
82 citing papers in PubMed, 132 citations in OpenAlex.
- Decoding the Oncogenic Role of USP22 Through Pan-Cancer Genomic and Epigenetic Analysis.Cancer reports (Hoboken, N.J.) · 2026Article
- Targeting ubiquitin-specific peptidase 22 in solid tumours: from ubiquitination to immunotherapy.Frontiers in cell and developmental biology · 2026Review
- Novel circRNA signatures in cervical cancer: implications for early detection and screening.Biomarkers in medicine · 2026Article
- Regulatory roles of five key USP family deubiquitinases in cancer: from mechanisms to targeted therapy advances.Frontiers in pharmacology · 2026Review
- Targeting USP22 to promote K63-linked ubiquitination and degradation of SARS-CoV-2 nucleocapsid protein.Journal of virology · 2025Article
- Hepatocyte growth factor promotes melanoma metastasis through ubiquitin-specific peptidase 22-mediated integrins upregulation.Cancer letters · 2024Article
- USP11 promotes prostate cancer progression by up-regulating AR and c-Myc activity.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Reciprocal regulation between RACGAP1 and AR contributes to endocrine therapy resistance in prostate cancer.Cell communication and signaling : CCS · 2024Article
- Drug resistance mechanisms and treatment strategies mediated by Ubiquitin-Specific Proteases (USPs) in cancers: new directions and therapeutic options.Molecular cancer · 2024Review
- USP22 regulates APL differentiation via PML-RARα stabilization and IFN repression.Cell death discovery · 2024Article
- Programmed Death Ligand 1 Regulatory Crosstalk with Ubiquitination and Deubiquitination: Implications in Cancer Immunotherapy.International journal of molecular sciences · 2024Review
- USP22 overexpression fails to augment tumor formation in MMTV-ERBB2 mice but loss of function impacts MMTV promoter activity.PloS one · 2024Article
- Deubiquitinases in cancer.Nature reviews. Cancer · 2023Review
- UPS writes a new saga of SAGA.Biochimica et biophysica acta. Gene regulatory mechanisms · 2023Review
- Inhibition of USP7 upregulates USP22 and activates its downstream cancer-related signaling pathways in human cancer cells.Cell communication and signaling : CCS · 2023Article
- Article
- Nuclear transport maintenance of USP22-AR by Importin-7 promotes breast cancer progression.Cell death discovery · 2023Article
- USP22 upregulates ZEB1-mediated VEGFA transcription in hepatocellular carcinoma.Cell death & disease · 2023Article
- USP22 suppresses the NLRP3 inflammasome by degrading NLRP3 via ATG5-dependent autophagy.Autophagy · 2023Article
- A review of deubiquitinases and thier roles in tumorigenesis and development.Frontiers in bioengineering and biotechnology · 2023Review
22 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 5 institutions in 2 countries.
Funding
Abstract
Increasing evidence links deregulation of the ubiquitin-specific proteases 22 (USP22) deubitiquitylase to cancer development and progression in a select group of tumor types, but its specificity and underlying mechanisms of action are not well defined. Here we show that USP22 is a critical promoter of lethal tumor phenotypes that acts by modulating nuclear receptor and oncogenic signaling. In multiple xenograft models of human cancer, modeling of tumor-associated USP22 deregulation demonstrated that USP22 controls androgen receptor accumulation and signaling, and that it enhances expression of critical target genes coregulated by androgen receptor and MYC. USP22 not only reprogrammed androgen receptor function, but was sufficient to induce the transition to therapeutic resistance. Notably, in vivo depletion experiments revealed that USP22 is critical to maintain phenotypes associated with end-stage disease. This was a significant finding given clinical evidence that USP22 is highly deregulated in tumors, which have achieved therapeutic resistance. Taken together, our findings define USP22 as a critical effector of tumor progression, which drives lethal phenotypes, rationalizing this enzyme as an appealing therapeutic target to treat advanced disease.
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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.