ArticleJournal of advanced research2025
HnRNPR-mediated UPF3B mRNA splicing drives hepatocellular carcinoma metastasis.
Article in Journal of advanced research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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13 citing papers in PubMed, 16 citations in OpenAlex.
- TGFβ1 Activates Lnc-APUE to Promote Tumor Metastasis via the Alu Element-Driven STAU1-Mediated Decay of CDH1 mRNA.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Characterization and therapy of fertilization failure in murine and human models with HNRNPR mutations.EMBO molecular medicine · 2026Article
- circ-UBR5 in hypoxia-induced exosomes may mediate lung adenocarcinoma metastasis via the targeting of HNRNPR.Translational lung cancer research · 2026Article
- Multiomic Detection of RNA, Protein, and Protein-Protein Proximity at Subcellular Resolution Using Automated Protease-Free RNAscope™ Workflows.Methods in molecular biology (Clifton, N.J.) · 2026Article
- Alternative Splicing: Molecular Mechanisms, Biological Functions, Diseases, and Potential Therapeutic Targets.MedComm · 2025Review
- RBM8A promotes gastric cancer progression by binding with UPF3B to induce BBC3 mRNA degradation.International journal of molecular medicine · 2025Article
- Sex-dependent epigenetic disruption of YY1 binding by prenatal BPA exposure downregulates Matr3 and alters Agap1 splicing in the offspring hippocampus.Biology of sex differences · 2025Article
- LncRNA MIR503HG regulates NETs-mediated NLRP3 inflammasome activation and NSCLC metastasis by enhancing the ubiquitination of C/EBPβ.Clinical and translational medicine · 2025Article
- Comprehensive bioinformatics analysis of MEX3 family genes in hepatocellular carcinoma.Scientific reports · 2025Article
- An evolutionarily conserved tryptophan cage promotes folding of the extended RNA recognition motif in the hnRNPR-like protein family.Protein science : a publication of the Protein Society · 2025Article
- Contributions of Folded and Disordered Domains to RNA Binding by HNRNPR.bioRxiv : the preprint server for biology · 2025Article
- SHMT2 modulates the transcriptome and metabolism profiles to promote the tumor phenotypes of bladder cancer HT-1376 cells.Frontiers in genetics · 2025Article
- Unveiling the role of UPF3B in hepatocellular carcinoma: Potential therapeutic target.Cancer science · 2024Article
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Authors and funding
17 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionAbnormal alternative splicing (AS) contributes to aggressive intrahepatic invasion and metastatic spread, leading to the high lethality of hepatocellular carcinoma (HCC).
objectivesThis study aims to investigate the functional implications of UPF3B-S (a truncated oncogenic splice variant) in HCC metastasis.
methodsBasescope assay was performed to analyze the expression of UPF3B-S mRNA in tissues and cells. RNA immunoprecipitation, and in vitro and in vivo models were used to explore the role of UPF3B-S and the underlying mechanisms.
resultsWe show that splicing factor HnRNPR binds to the pre-mRNA of UPF3B via its RRM2 domain to generate an exon 8 exclusion truncated splice variant UPF3B-S. High expression of UPF3B-S is correlated with tumor metastasis and unfavorable overall survival in patients with HCC. The knockdown of UPF3B-S markedly suppresses the invasive and migratory capacities of HCC cells in vitro and in vivo. Mechanistically, UPF3B-S protein targets the 3'-UTR of CDH1 mRNA to enhance the degradation of CDH1 mRNA, which results in the downregulation of E-cadherin and the activation of epithelial-mesenchymal transition. Overexpression of UPF3B-S enhances the dephosphorylation of LATS1 and the nuclear accumulation of YAP1 to trigger the Hippo signaling pathway.
conclusionOur findings suggest that HnRNPR-induced UPF3B-S promotes HCC invasion and metastasis by exhausting CDH1 mRNA and modulating YAP1-Hippo signaling. UPF3B-S could potentially serve as a promising biomarker for the clinical management of invasive HCC.
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