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Unveiling NUSAP1 as a common gene signature linking chronic HBV infection and HBV-related HCC
Jiao Meng1, Zhenkun Yang1, Xinyi Jiang2
1Department of Laboratory Medicine, The Affiliated Wuxi People's Hospital of Nanjing Medical University, Wuxi People's Hospital, Wuxi Medical Center, Nanjing Medical University, 299 Qingyang Road, Wuxi, 214023, Jiangsu, China.
Insights
Hepatitis B virus (HBV) infection can lead to liver cancer. Researchers identified NUSAP1 as a key gene promoting cancer growth and inhibiting cell death, indicating it
Area of Science:
- Hepatology
- Oncology
- Bioinformatics
Background:
- Hepatitis B virus (HBV) infection is a major risk factor for hepatocellular carcinoma (HCC).
- Mechanisms driving HBV infection progression to HCC are not fully understood.
- Identifying key molecular players is crucial for understanding HBV-related HCC pathogenesis.
Purpose of the Study:
- To identify a hub gene connecting chronic HBV infection (CHB) and HBV-related HCC.
- To elucidate the role of this hub gene in liver cancer progression.
Main Methods:
- Bioinformatic analysis of gene expression datasets (GEO database).
- Identification of differentially expressed genes (DEGs) and pathway enrichment (GO, KEGG).
- Protein-protein interaction (PPI) network analysis (Cytoscape) to screen hub genes.
- Prognostic assessment and functional experiments (cell growth, apoptosis) for validation.
Main Results:
- NUSAP1 was found to be upregulated in both CHB and HBV-HCC patients.
- High NUSAP1 expression is an independent predictor of poor prognosis in liver cancer.
- NUSAP1 promotes cell proliferation, cell cycle progression, and inhibits apoptosis in liver cancer cells.
Conclusions:
- NUSAP1 is a significant prognostic indicator for liver cancer.
- NUSAP1 plays a critical role in HBV-HCC progression by enhancing cell proliferation and reducing apoptosis.
Background:
Hepatitis B virus (HBV) is a significant contributor to the development of hepatocellular carcinoma (HCC). Chronic HBV infection (CHB) facilitates disease progression through various mechanisms. However, the specific factor responsible for the progression of HBV infection to HCC remains unresolved. This study aims to identify the hub gene linking CHB and HBV-related HCC through bioinformatic analysis and experimental verification.
Methods:
Differentially expressed genes (DEGs) were identified in datasets encompassing CHB and HBV-HCC patients from the GEO database. Enriched pathways were derived from GO and KEGG analysis. Hub genes were screened by protein-protein interaction (PPI) analysis and different modules in Cytoscape software. The significance of the selected hub gene in prognosis was further assessed in validated datasets. The effects of hub genes on cell growth and apoptosis were further determined in functional experiments.
Results:
The study revealed upregulation of NUSAP1 in CHBs and HBV-HCCs. High expression of NUSAP1 served as an independent predictor for poor prognosis of liver cancers. Functional experiments demonstrated that NUSAP1 promotes cell growth, influences cell cycle process, and protects cells from apoptosis in HepG2.2.15 cells.
Conclusion:
NUSAP1 serves as a poor prognostic indicator for liver cancers, and potentially plays a crucial role in HBV-HCC progression by promoting proliferation and inhibiting apoptosis.
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