ArticleOncoTargets and therapy2020
Pre-mRNA Processing Factor 8 Accelerates the Progression of Hepatocellular Carcinoma by Regulating the PI3K/Akt Pathway.
Article in OncoTargets and therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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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Who cites it
3 citing papers in PubMed, 11 citations in OpenAlex.
- Research Progress on the Relationship Between PRPF8 and Cancer.Current issues in molecular biology · 2025Review
- Altered splicing machinery in lung carcinoids unveils NOVA1, PRPF8 and SRSF10 as novel candidates to understand tumor biology and expand biomarker discovery.Journal of translational medicine · 2023Article
- PRPF8 increases the aggressiveness of hepatocellular carcinoma by regulating FAK/AKT pathway via fibronectin 1 splicing.Experimental & molecular medicine · 2023Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe specific function of pre-mRNA processing factors (Prps) in human malignancies has not been yet investigated. The aim of the present study was to determine the impacts of Prp8 in a common human malignancy, hepatocellular carcinoma (HCC). MATERIALS AND
methodsRT-qPCR and Western blotting were performed to measure the expression levels of Prp8 in various HCC cell lines and HCC tissues. A hepatic astrocyte line was transfected with a eukaryotic expression plasmid to overexpress Prp8. In addition, the endogenous expression level of Prp8 in HCC cells was silenced using a short hairpin RNA method, and the role of Prp8 on cell proliferation and migration was examined by Cell Counting Kit-8, wound healing assay and Transwell assays following knockdown in HCC cells, and overexpression in astrocytes.
resultsUpregulation of Prp8 expression was found to be associated with poor clinical outcomes in patients with HCC. The upregulation of Prp8 promoted cell viability, metastasis and the activity of the PI3K/Akt pathway in hepatic astrocytes cells and HCC cells. Interestingly, loss of Prp8 had no obvious impact on cell viability and migration in hepatic astrocytes, but significantly inhibit the cell malignancy of HCC cells. Functionally, the inhibition of the PI3K/Akt pathway reversed the increased cell viability and migration of HCC cells induced by Prp8 via inhibiting EMT process.
conclusionCollectively, the present results suggested that Prp8 served as a tumor promoter in HCC by targeting and regulating the PI3K/Akt pathway.
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