ArticleExperimental & molecular medicine2023
PRPF8 increases the aggressiveness of hepatocellular carcinoma by regulating FAK/AKT pathway via fibronectin 1 splicing.
Article in Experimental & molecular medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
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Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.
- Decoding the role of aberrant RNA alternative splicing in hepatocellular carcinoma: a comprehensive review.Journal of cancer research and clinical oncology · 2023Pooled it
- Spatial transcriptomics uncovers TAC-OGEs heterogeneity and FN1/MMP9 signature in ameloblastoma.Frontiers in immunology · 2026Article
- Integrative RNA-seq and iRIP-seq analysis links SNRPA overexpression to transcriptomic and splicing alterations in hepatocellular carcinoma cells.Frontiers in oncology · 2026Article
- Decoding retinitis pigmentosa: molecular targets and therapy with focus on pre-mRNA splicing.Cellular and molecular life sciences : CMLS · 2025Review
- Comprehensive single-cell transcriptome landscape of metastatic colorectal cancer identifies budding-potential cells and their interactions with cancer-associated fibroblasts.NPJ precision oncology · 2025Article
- Impaired splicing machinery in craniopharyngiomas unveils PRPF8 and RAVER1 as novel biomarkers and therapeutic targets.Acta neuropathologica communications · 2025Article
- Extracellular matrix: unlocking new avenues in cancer treatment.Biomarker research · 2025Review
- Research Progress on the Relationship Between PRPF8 and Cancer.Current issues in molecular biology · 2025Review
- Quantitative proteomic analysis unveils a critical role of VARS1 in hepatocellular carcinoma aggressiveness through the modulation of MAGI1 expression.Molecular cancer · 2025Article
- Proteomic Characterization of Liver Cancer Cells Treated with Clinical Targeted Drugs for Hepatocellular Carcinoma.Biomedicines · 2025Article
- Review
- A de novoHormone research in paediatrics · 2025Article
- Schisandrin B downregulates exosomal fibronectin 1 expression to inhibit hepatocellular carcinoma growth.Frontiers in pharmacology · 2025Article
- Article
- CancerHubs: a systematic data mining and elaboration approach for identifying novel cancer-related protein interaction hubs.Briefings in bioinformatics · 2024Article
- Integrated Lactylome Characterization Reveals the Molecular Dynamics of Protein Regulation in Gastrointestinal Cancers.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Biological impact and therapeutic implication of tumor-associated macrophages in hepatocellular carcinoma.Cell death & disease · 2024Review
- Oncofetal SNRPE promotes HCC tumorigenesis by regulating the FGFR4 expression through alternative splicing.British journal of cancer · 2024Article
- Proteomics Identifies LUC7L3 as a Prognostic Biomarker for Hepatocellular Carcinoma.Current issues in molecular biology · 2024Article
- Article
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Authors and funding
14 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatocellular carcinoma (HCC) pathogenesis is associated with alterations in splicing machinery components (spliceosome and splicing factors) and aberrant expression of oncogenic splice variants. We aimed to analyze the expression and potential role of the spliceosome component PRPF8 (pre-mRNA processing factor 8) in HCC. PRPF8 expression (mRNA/protein) was analyzed in a retrospective cohort of HCC patients (n = 172 HCC and nontumor tissues) and validated in two in silico cohorts (TCGA and CPTAC). PRPF8 expression was silenced in liver cancer cell lines and in xenograft tumors to understand the functional and mechanistic consequences. In silico RNAseq and CLIPseq data were also analyzed. Our results indicate that PRPF8 is overexpressed in HCC and associated with increased tumor aggressiveness (patient survival, etc.), expression of HCC-related splice variants, and modulation of critical genes implicated in cancer-related pathways. PRPF8 silencing ameliorated aggressiveness in vitro and decreased tumor growth in vivo. Analysis of in silico CLIPseq data in HepG2 cells demonstrated that PRPF8 binds preferentially to exons of protein-coding genes, and RNAseq analysis showed that PRPF8 silencing alters splicing events in multiple genes. Integrated and in vitro analyses revealed that PRPF8 silencing modulates fibronectin (FN1) splicing, promoting the exclusion of exon 40.2, which is paramount for binding to integrins. Consistent with this finding, PRPF8 silencing reduced FAK/AKT phosphorylation and blunted stress fiber formation. Indeed, HepG2 and Hep3B cells exhibited a lower invasive capacity in membranes treated with conditioned medium from PRPF8-silenced cells compared to medium from scramble-treated cells. This study demonstrates that PRPF8 is overexpressed and associated with aggressiveness in HCC and plays important roles in hepatocarcinogenesis by altering FN1 splicing, FAK/AKT activation and stress fiber formation.
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