ArticleClinical cancer research : an official journal of the American Association for Cancer Research2020
Deubiquitinase Activity Profiling Identifies UCHL1 as a Candidate Oncoprotein That Promotes TGFβ-Induced Breast Cancer Metastasis.
Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers.
What it found
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Who cites it
104 citing papers in PubMed, 172 citations in OpenAlex.
- It takes two to tango: the intersection of deubiquitinases and mMolecular cancer · 2026Review
- Review
- The Deubiquitinase UCHL1 Drives Susceptibility to Atrial Fibrillation by Stabilizing CaMKII-δ.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- UCHL1 Promotes M1 Macrophage Polarization and Inflammation in Chronic Rhinosinusitis by Stabilizing HIF-1α.Cell biochemistry and biophysics · 2026Article
- UCHL1-mediated deubiquitination of PARK7 suppresses ferroptosis and enhances tumor progression in triple-negative breast cancer.Molecular and cellular biochemistry · 2026Article
- Tied to Work: Topologically Knotted SPOUT Methyltransferases and UCH Deubiquitinases in Cellular Biochemistry.Journal of cellular biochemistry · 2026Review
- EIF3H Modulates Glycolysis Through LDHA Stabilization in Triple-Negative Breast Cancer.Cancers · 2026Article
- UCH-L1 down-regulates HER2 expression and increases lapatinib sensitivity by interacting with HSP90 in HER2-positive breast cancer.Genes & diseases · 2026Article
- UCHL1-mediated deubiquitination of GLOD4 regulates mitochondrial homeostasis and PTC malignant progression via GLO1.Molecular and cellular biochemistry · 2026Article
- circTGFBR2(3-6) acts as an assembly platform for RNA-binding protein IGF2BP3 and TGFBR1 mRNA to enhance breast cancer cell plasticity.Cell death and differentiation · 2026Article
- Deubiquitinase UCH-L1 confers paclitaxel resistance via stabilizing PKM2 to promote glycolysis in triple-negative breast cancer.Cell death & disease · 2026Article
- Proteomics analysis of serum extracellular vesicle identifies UCHL1 as a potential therapeutic target for high grade serous ovarian cancer.British journal of cancer · 2026Article
- Ubiquitination modifications as central regulators of metabolic dysfunction in type 2 diabetes mellitus.Frontiers in endocrinology · 2026Review
- Potential Anti-Cancer Drug 6RK73 Suppresses Ovarian Cancer Growth by Inactivating the AKT1/Sp1 Induced c-Myc Signaling Pathway.Journal of Cancer · 2026Article
- Article
- Carbonic Anhydrase Inhibition Sensitizes Group 3 Medulloblastoma to Radiotherapy.Cancer research · 2025Article
- UCHL3: a crucial deubiquitinase in DNA damage repair and tumor progression.Cancer cell international · 2025Review
- Ubiquitin C-terminal hydrolase L1 promoted pro-angiogenic capacity of periodontal ligament stem cells via HIF-1α/YAP signaling in periodontitis.Stem cell research & therapy · 2025Article
- Role of Triple-Negative Breast Cancer-Derived Extracellular Vesicles in Metastasis: Implications for Therapeutics and Biomarker Development.Journal of cellular and molecular medicine · 2025Review
- Article
44 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
19 authors at 5 institutions in 3 countries.
Funding
Abstract
purposeTherapies directed to specific molecular targets are still unmet for patients with triple-negative breast cancer (TNBC). Deubiquitinases (DUB) are emerging drug targets. The identification of highly active DUBs in TNBC may lead to novel therapies. EXPERIMENTAL
designUsing DUB activity probes, we profiled global DUB activities in 52 breast cancer cell lines and 52 patients' tumor tissues. To validate our findings
resultsTwo DUB activity profiling approaches identified UCHL1 as being highly active in TNBC cell lines and aggressive tumors. Functionally, UCHL1 promoted metastasis in zebrafish and murine breast cancer xenograft models. Mechanistically, UCHL1 facilitates TGFβ signaling-induced metastasis by protecting TGFβ type I receptor and SMAD2 from ubiquitination. We found that these responses are potently suppressed by the specific UCHL1 inhibitor, 6RK73. Furthermore, UCHL1 levels were significantly increased in sera of patients with TNBC, and highly enriched in sera exosomes as well as TNBC cell-conditioned media. UCHL1-enriched exosomes stimulated breast cancer migration and extravasation, suggesting that UCHL1 may act in a paracrine manner to promote tumor progression.
conclusionsOur DUB activity profiling identified UCHL1 as a candidate oncoprotein that promotes TGFβ-induced breast cancer metastasis and may provide a potential target for TNBC treatment.
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