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Updated: May 11, 2025

Isolation of Primary Mouse Hepatocytes for Nascent Protein Synthesis Analysis by Non-radioactive L-azidohomoalanine Labeling Method
Published on: October 23, 2018
Decoding the role of nucleic acid binding protein 2 in lipid dysregulation and hepatocellular carcinoma progression
Chengchen Dai1, Yun Tong2, Nan Bai1
1Research Center of Clinical Medicine & Department of Clinical and Translational Research Center, Affiliated Hospital of Nantong University, Medical School of Nantong University, Nantong 226001, China; Department of Oncology, Affiliated Hospital of Nantong University, Medical School of Nantong University, Nantong 226001, China.
Abstract:
Nucleic Acid Binding Protein 2 (NABP2), a crucial regulator in the single-stranded DNA-binding protein family, has been linked to the progression of hepatocellular carcinoma (HCC) and poor prognosis. However, the precise mechanisms by which NABP2 regulates HCC development, especially through metabolic pathways, remain unclear. In this study, we evaluated NABP2 expression in clinical HCC samples and analyzed its correlation with patient survival outcomes. Functional assays, including cell proliferation, migration, and lipid metabolism analyses, were performed in vitro and in vivo to investigate the role of NABP2 in tumorigenesis. Additionally, we examined the molecular interactions of NABP2 with the E3 ubiquitin ligase STUB1 and its impact on the LKB1/AMPK signaling pathway. Our results revealed that NABP2 was overexpressed in HCC tissues and associated with worse survival outcomes. NABP2 promoted tumor cell proliferation, migration, and disrupted lipid metabolism. Mechanistically, NABP2 regulated the proteostasis of liver kinase B1 (LKB1) by recruiting STUB1, leading to the inhibition of the LKB1/AMPK signaling axis and mitochondrial dysfunction. In conclusion, our findings suggest that NABP2 may serve as both a biomarker and a potential therapeutic target for HCC, offering novel insights into its role in metabolic reprogramming and tumor progression.
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