ArticleBiomedicines2022
UPF1 Inhibits Hepatocellular Carcinoma Growth through DUSP1/p53 Signal Pathway.
Article in Biomedicines, 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- Suppressor with morphogenetic effect on genitalia 7 (SMG7) drives hepatocellular carcinoma progression through context-dependent nonsense-mediated decay (NMD) dysregulation.Molecular biomedicine · 2026Article
- Review
- Early growth response 1 regulates dual‑specificity protein phosphatase 1 and inhibits cell migration and invasion of tongue squamous cell carcinoma.Oncology letters · 2024Article
- Role of UPF1 in lncRNA-HEIH regulation for hepatocellular carcinoma therapy.Experimental & molecular medicine · 2024Article
- Identification of Genes Involved in EGF-induced Apoptosis Using CRISPR/Cas9 Knockout Screening: Implications for Novel Therapeutic Targets in EGFR-Overexpressing Cancers.Cancer research and treatment · 2023Article
- Identification and Validation of UPF1 as a Novel Prognostic Biomarker in Renal Clear Cell Carcinoma.Genes · 2022Article
- mRNA Metabolism in Health and Disease.Biomedicines · 2022Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human hepatocellular carcinoma (HCC) has a high mortality rate because of the dearth of effective treatments. Multiple studies have shown that overexpression of UPF1, a key nonsense-mediated mRNA decay (NMD) factor, reduces HCC growth through various cell signaling pathways. However, the mechanism by which UPF1 expression retards HCC proliferation through the regulation of RNA stability remains unclear. By employing various UPF1 variants and transcriptome analysis, we revealed that overexpression of UPF1 variants, not UPF1-mediated NMD, reduces HCC tumorigenesis. Additionally, UPF1 variant overexpression reduced tumorigenesis in xenografted mice. Transcriptome analysis indicated that the level of dual specificity phosphatase 1 (DUSP1) was increased by UPF1 variants via posttranscriptional regulation. The UPF1 overexpression-mediated increase of DUSP1 activated tumor suppressor signaling, ultimately inhibiting cell growth. In this study, we highlighted the function of UPF1 as a tumor suppressor in HCC growth.
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Registered trials
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