Japan Digestive Disease Week 2025
International Poster Session12 (JDDW)
October 31, 14:32–15:20, Room 15 (Kobe International Exhibition Hall No.1 Building Digital Poster Venue)
IP-55_H
Functional Analysis of Hepatocyte Host Factor A1BG in Antiviral and Antitumor Effects in HBV-transfected HepG2 cells
- 1
- Second Department of Internal Medicine, University of Fukui
- 2
- Shaoxing People's Hospital, Department of Clinical Laboratory
Background
Hepatitis B virus (HBV) causes over 50% of virus-related Hepatocellular carcinoma (HCC). Host factors play crucial roles in HBV-related HCC progression. Our previous study identified alpha-1-B glycoprotein (A1BG) as a candidate host factor in regulating HBV infection (PLOS One 2025). We explored the anti-HBV and antitumor effects of A1BG.
Methods
A1BG expression in HCC was analyzed using TCGA-LIHC and GSE121248 datasets. DEGs between high and low A1BG groups were identified using DESeq2. HepG2.1-E10 (Low HBV transcription) and HepG2.D11 (High HBV t.) cell lines, transfected with HBV genotype C2 genome, were used to study A1BG's effects. siRNA and plasmid vectors were used to knockdown and overexpression A1BG. MTT, CFSE, Annexin V/PI, wound healing, and transwell assays evaluated cell proliferation, apoptosis, migration, and invasion.
Results
A1BG expression was lower in HCC samples than in adjacent tissues. Lower A1BG expression correlated with higher pathological stage and poorer overall survival. A1BG-related DEGs were enriched in Wnt signaling pathway and extracellular matrix. Overexpression of A1BG reduced HBV-RNA levels, suppressed cell proliferation, increased apoptosis, and inhibited cell migration and invasion, while knockdown showed opposite effects.
Conclusions
A1BG regulates viral production and tumor progression in HepG2 cells transfected with HBV genome, highlighting its potential as a therapeutic target for HBV-related HCC.
Hepatitis B virus (HBV) causes over 50% of virus-related Hepatocellular carcinoma (HCC). Host factors play crucial roles in HBV-related HCC progression. Our previous study identified alpha-1-B glycoprotein (A1BG) as a candidate host factor in regulating HBV infection (PLOS One 2025). We explored the anti-HBV and antitumor effects of A1BG.
Methods
A1BG expression in HCC was analyzed using TCGA-LIHC and GSE121248 datasets. DEGs between high and low A1BG groups were identified using DESeq2. HepG2.1-E10 (Low HBV transcription) and HepG2.D11 (High HBV t.) cell lines, transfected with HBV genotype C2 genome, were used to study A1BG's effects. siRNA and plasmid vectors were used to knockdown and overexpression A1BG. MTT, CFSE, Annexin V/PI, wound healing, and transwell assays evaluated cell proliferation, apoptosis, migration, and invasion.
Results
A1BG expression was lower in HCC samples than in adjacent tissues. Lower A1BG expression correlated with higher pathological stage and poorer overall survival. A1BG-related DEGs were enriched in Wnt signaling pathway and extracellular matrix. Overexpression of A1BG reduced HBV-RNA levels, suppressed cell proliferation, increased apoptosis, and inhibited cell migration and invasion, while knockdown showed opposite effects.
Conclusions
A1BG regulates viral production and tumor progression in HepG2 cells transfected with HBV genome, highlighting its potential as a therapeutic target for HBV-related HCC.
- Index Term 1: A1BG
- Index Term 2: Hepatocyte Host Factor