ArticleOncogene2025
PABPN1-C5 axis promotes hepatocellular carcinoma progression via NF-κB activation.
Article in Oncogene, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed.
- PABPC1 in Cancer: From a Translational Housekeeper to a Stress-Responsive Regulatory Hub.Cancer science · 2026Review
- Macrophage PABPC4-SPP1 Axis Orchestrates Immunosuppression in Colorectal Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Neutrophils: emerging perspectives on the pathogenesis of oral mucosal diseases.Frontiers in cellular and infection microbiology · 2025Review
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
RNA polyadenylation is a key post-transcriptional modification essential for gene expression regulation. However, the role and mechanism of polyadenylation and its key molecule, polyadenylate binding protein nuclear 1 (PABPN1), in hepatocellular carcinoma (HCC) remain poorly understood. This study investigates the role of PABPN1 and its regulatory genes in HCC progression to identify potential therapeutic targets. Analysis of The Cancer Genome Atlas (TCGA) dataset and an independent HCC cohort revealed significant upregulation of PABPN1 in HCC patients, which correlates with poor prognosis. Loss-of-function studies using HCC cell lines and conditional knockout mouse models demonstrated that targeting PABPN1 inhibited HCC progression. Conversely, overexpression of PABPN1 promoted HCC development in vitro and in a hydrodynamic transfection hepatocarcinogenesis mouse model. Mechanistic investigations showed that PABPN1 modulates C5 mRNA polyadenylation and stability, with the PABPN1-C5 axis driving NF-κB activation and recruiting polymorphonuclear myeloid-derived suppressor cells (PMN-MDSCs) to promote HCC progression. Therapeutic targeting of the PABPN1-C5 axis using the C5a receptor inhibitor CCX168 significantly inhibited HCC progression in both in vitro and in vivo models. This study identifies PABPN1 as a critical regulator of HCC development and sheds light on the post-transcriptional regulation of complement components in cancer. Targeting the PABPN1-C5 axis represents a promising strategy for HCC treatment.
Indexed as
Identifiers
40721660What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.