NARS1 Enhances HCC Proliferation by Stimulating NF‐ <i>κ</i> B Signaling Pathway
Background Hepatocellular carcinoma (HCC) is still an important risk to public health, and its pathogenesis is still unclear. Therefore, it is important to probe the HCC pathogenesis and constantly find new diagnostic and therapeutic targets in HCC markers. Materials and Methods TCGA database, western blot, and qPCR were used to identify the role of NARS1 in tumor tissues from HCC tumor tissues. Co‐immunoprecipitation was used to investigate the direct interaction between NARS1 and HuR. Pulldown assays, co‐expression plasmid, and dual‐luciferase reporter gene assays were identified to investigate the role of NARS1 in NF‐ κ B signaling pathway. Results In the present study, we demonstrated that NARS1 promotes HCC proliferation and the potential target for diagnosis and treatment of HCC. Through multicohort analysis, the expression of NARS1 in HCC was significantly upregulated, and NARS1 expression in tumor tissues was positively correlated with the poor prognosis of patients. NARS1 can activate the NF‐ κ B signaling pathway by forming heterodimers with HuR, which further enhanced HCC proliferation. Conclusions Collectively, these studies reveal the intrinsic mechanism by which NARS1 promotes HCC proliferation and impart a potential rationale for the subsequent NARS1 clinical translational application.
Authors
- Hexu Han (ORCID: https://orcid.org/0000-0002-5812-0123)
- Ping Huang (ORCID: https://orcid.org/0000-0003-1775-029X)
- Heng Guo (ORCID: https://orcid.org/0000-0002-6769-919X)
- Lingjian Li
- Cuixia Liu
- Dakun Zhao
- Yin Yuan
Institutions
- Nantong University (CN)
- Affiliated Hospital of Nantong University (CN)
- Nanjing Drum Tower Hospital (CN)
- Second People's Hospital of NanTong (CN)
- The Affiliated Taizhou People's Hospital of Nanjing Medical University (CN)
Publication Details
- Journal
- Human Mutation
- Published
- 2026-01-01
- DOI
- https://doi.org/10.1155/humu/8809532
- Primary Topic
- Signaling Pathways in Disease
- Type
- article
- Field-Weighted Citation Impact
- 0.00