ArticleAmerican journal of clinical and experimental urology2024
Ubiquitin C-terminal hydrolase L1 is a regulator of tumor growth and metastasis in double-negative prostate cancer.
Article in American journal of clinical and experimental urology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Deubiquitinating enzymes in cervical cancer: Molecular mechanisms and therapeutic implications (Review).International journal of oncology · 2026Review
- Deciphering double-negative prostate cancer: from aggressive subtype to novel therapeutic paradigms.Cell communication and signaling : CCS · 2026Review
- Proteomics analysis of serum extracellular vesicle identifies UCHL1 as a potential therapeutic target for high grade serous ovarian cancer.British journal of cancer · 2026Article
- Expression of ubiquitin carboxyl-terminal hydrolase isozyme L1 and chromogranin A regulated via histone-modification through Rho/ERK/NFκB signaling in oxaliplatin-resistant colorectal cancer cells.International journal of medical sciences · 2026Article
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Authors and funding
6 authors.
Funding
Abstract
Prostate cancer is the second leading cause of cancer-related deaths among men worldwide. With heavy androgen deprivation therapies, prostate cancer may shift to androgen receptor negative and neuroendocrine negative subtype of castration resistant prostate cancer, defined as double-negative prostate cancer. Double-negative prostate cancer is associated with poor prognosis and disease mortality. The molecular mechanisms underlying the emergence of double-negative prostate cancer remain poorly understood. Here, we demonstrate that Ubiquitin C-Terminal Hydrolase L1 (UCH-L1), is negatively correlated with androgen receptor levels in prostate cancer patients. UCH-L1 plays a functional role in tumorigenesis and metastasis in double-negative prostate cancer. Knock-down of UCH-L1 decreases double-negative prostate cancer colony formation
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