ArticleJournal of molecular histology2021
Ubiquitin-specific protease 14 (USP14) promotes proliferation and metastasis in pancreatic ductal adenocarcinoma.
Article in Journal of molecular histology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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Who cites it
9 citing papers in PubMed, 10 citations in OpenAlex.
- The multifaceted roles of deubiquitinating enzymes (DUBs) in pancreatic ductal adenocarcinoma.Cell death & disease · 2025Review
- USP14 Mediates Molecular Mechanisms Regulating Aortic Valve Stenosis Through Ubiquitination.Journal of cellular and molecular medicine · 2025Article
- USP14/S100A11 axis promote colorectal cancer progression by inhibiting cell senescence.Cell death & disease · 2025Article
- Article
- A self-amplifying USP14-TAZ loop drives the progression and liver metastasis of pancreatic ductal adenocarcinoma.Cell death and differentiation · 2023Article
- USPs in Pancreatic Ductal Adenocarcinoma: A Comprehensive Bioinformatic Analysis of Expression, Prognostic Significance, and Immune Infiltration.BioMed research international · 2022Article
- The role of ubiquitination and deubiquitination in tumor invasion and metastasis.International journal of biological sciences · 2022Review
- Small-Molecule Inhibitors Targeting Proteasome-Associated Deubiquitinases.International journal of molecular sciences · 2021Review
- The prognostic value of USP14 and PSMD14 expression in non-small cell lung cancer.Annals of translational medicine · 2021Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Previous studies have shown aberrant expression of ubiquitin-specific protease 14 (USP14) in multiple malignancies, suggesting an important role of USP14 in tumorigenesis. However, the functional role of USP14 in pancreatic ductal adenocarcinoma (PDAC) has never been elucidated. In this study, we found that USP14 was remarkably upregulated in PDAC tissues compared with normal pancreatic tissues. Notably, Kaplan-Meier curves showed that high expression of USP14 predicted significantly worse prognosis in PDAC patients than low expression of USP14. To determine whether USP14 could regulate the proliferation, apoptosis and metastasis of PDAC cells, we knocked down endogenous USP14 or overexpressed exogenous USP14 in Panc-1 and BxPC-3 cells. Using MTT assays, colony formation analyses, flow cytometry assays, and cell invasion and migration assays, we found that knockdown of USP14 attenuated proliferation, induced apoptosis and restrained invasion and migration of PDAC cells. Overexpression of USP14 could enhance proliferation, prevent apoptosis and promote invasion and migration of PDAC cells. In addition, USP14 could regulate the expression of cyclin D1, PCNA and E-cadherin, three important carcinogenic factors, in PDAC cells. These findings suggest that USP14 might play an important role in promoting the tumorigenesis of PDAC and thus be a promising therapeutic target to prevent PDAC progression.
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Registered trials
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