ArticleFrontiers in oncology2023
UCA1 executes an oncogenic role in pancreatic cancer by regulating miR-582-5p/BRCC3.
Article in Frontiers in oncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 7 citations in OpenAlex.
- Article
- Exploratory Multi-Platform Bioinformatic Analysis of MEAK7 and Its Molecular, Survival, and Immune Associations in Pancreatic Ductal Adenocarcinoma.International journal of molecular sciences · 2026Article
- BRCC3 promotes progression and immune evasion in non-small cell lung cancer through regulation of PD-L1 and B7-H3.Journal of molecular histology · 2026Article
- β-Asarone Inhibits Carboplatin Resistance in Retinoblastoma Cells Through the UCA1/miR-206/NRP1 Axis.Biochemical genetics · 2025Article
- Prognostic model establishment and immune microenvironment analysis based on transcriptomic data of long-term survivors of pancreatic ductal adenocarcinoma.Biochemistry and biophysics reports · 2025Article
- Therapeutic potential of hAMSCs in ligament regeneration: insights from the UCA1-miR-16-5p-FGF2 pathway.Stem cell research & therapy · 2025Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: As a fatal disease, the mechanism of pancreatic cancer is unclear. Urothelial carcinoma antigen 1(UCA1), a long noncoding RNA (lncRNA) that was first reported in bladder cancer, acts as an oncogene. However, the regulatory role and mechanism of UCA1 in pancreatic cancer remain unknown. This study aims to investigate the expression level and prognostic value of UCA1 in pancreatic cancer tissues, the effects and mechanism of UCA1 in regulating cell proliferation, apoptosis and metastasis. Methods: UCA1 expression levels in tissues were detected by in situ hybridization (ISH) and the prognostic value was evaluated by univariate and multivariate survival analysis. For Results: ISH staining revealed that UCA1 levels between cancer tissues (n=94) and tumor-adjacent tissues (n=73) did not show significant differences. Survival analysis indicated that high expression of UCA1 was an unfavorable prognosis factor for pancreatic cancer. Downregulation of UCA1 by siRNA significantly inhibited cell proliferation, decreased the capacities of cell migration and invasion, induced cell apoptosis, and inhibited EMT. Furthermore, we demonstrated that UCA1 positively regulated the expression of BRCC3 by inhibiting miR-582-5p. Rescue experiments indicated that either inhibiting the expression of miR-582-5p or enhancing expression of BRCC3 could partly attenuate the antitumor effects of downregulation of UCA1. Conclusion: UCA1 acted as an oncogene in pancreatic cancer by partly regulating miR-582-5p/BRCC3, which could be a new therapeutic target for pancreatic cancer.
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