ArticleHuman cell2022
Knockdown of UCHL3 inhibits esophageal squamous cell carcinoma progression by reducing CRY2 methylation.
Article in Human cell, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- Circadian clock and cancer.Military Medical Research · 2026Review
- UCHL3: a crucial deubiquitinase in DNA damage repair and tumor progression.Cancer cell international · 2025Review
- Integrated machine learning constructed a circadian-rhythm-related model to assess clinical outcomes and therapeutic advantages in hepatocellular carcinoma.Translational cancer research · 2025Article
- UCHL3 promotes hepatocellular carcinoma progression by stabilizing EEF1A1 through deubiquitination.Biology direct · 2024Article
- UCHL3 induces radiation resistance and acquisition of mesenchymal phenotypes by deubiquitinating POLD4 in glioma stem cells.Cellular and molecular life sciences : CMLS · 2024Article
- Activation of CTNNB1 by deubiquitinase UCHL3-mediated stabilization facilitates bladder cancer progression.Journal of translational medicine · 2023Article
- CircZNF367 promotes osteoclast differentiation and osteoporosis by interacting with FUS to maintain CRY2 mRNA stability.Journal of orthopaedic surgery and research · 2023Article
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
UCHL3 (Ubiquitin carboxyl-terminal hydrolase L3), a member of deubiquitinating enzymes, has been implicated in various cancers. However, the role of UCHL3 in esophageal squamous cell carcinoma (ESCC) remains unknown. In the current study, we aimed to investigate the role of UCHL3 in ESCC growth and migration, and whether UCHL3 could modulate CRY2 methylation through FOXM1. The expression of UCHL3 and CRY2 in ESCC tissues was assessed using qRT-PCR, western blotting and immunohistochemistry (IHC). Cell viability was determined by CCK-8 and colony formation assays. Hoechst 33342 and flow cytometry were used to detect cell apoptosis. Transwell assay was performed to investigate cell migration and invasion. In vivo animal model was used to assess cell tumorigenesis. Methylation-Specific PCR (MSP) was applied to detect CRY2 methylation in the promoter region. The results showed that UCHL3 expression was elevated in ESCC tissues and cells, while CRY2 expression was decreased. UCHL3 silencing inhibited cell viability, invasion, migration and induced cell apoptosis in vitro, repressed tumor growth in vivo, and increased CRY2 expression and decreased FOXM1 expression. In addition, UCHL3 knockdown decreased CRY2 methylation through downregulating FOXM1, leading to an increase in the expression of CRY2. Moreover, CRY2 silencing abolished UCHL3 deficiency-mediated inhibition in cell growth and migration. In summary, this study reveals that knockdown of UCHL3 inhibits ESCC growth and migration by reducing CRY2 methylation through downregulation of FOXM1 expression.
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