EP300 Modulates MCM8 Transcription and Augments the Malignant Phenotype of Hepatitis B Virus–Positive Hepatocellular Carcinoma Cells
Year: 2025
Type: article
Abstract: Chronic infection with the hepatitis B virus (HBV) remains one of the primary drivers of the development of hepatocellular carcinoma (HCC), a highly aggressive malignancy with a grim prognosis. This study focused on the role of E1A-binding protein p300 (EP300) in the malignant phenotype of HBV-positive HCC cells and its functional mechanism. Increased EP300 expression was detected in HBV-positive tumor tissues and cells compared to their control counterparts. Silencing EP300 reduced tumorigenic activity, proliferation, viability, migration, invasion, and resistance to apoptosis of HBV-positive cells and reduced the concentrations of HBV infection markers HBsAg and HBeAg. These effects were achieved, at least in part, through downregulation of minichromosome maintenance 8 homologous recombination repair factor (MCM8). MCM8 was identified as a target of EP300 and mediated by acetylation modification. MCM8 was upregulated in HBV-positive tumors and HCC cells while decreasing following EP300 silencing in cells. However, the restoration of MCM8 expression in these cells rescued their malignant properties. In summary, this study suggests a role for EP300-mediated MCM8 upregulation in the malignant properties of HBV-positive HCC.
DOI: 10.1002/kjm2.70006
Authors: Fang Xue, Tian‐Feng Sun
Institution: Suzhou Traditional Chinese Medicine Hospital
Language: English
Topic: Hepatitis B Virus Studies
Subfield: Epidemiology
Field: Medicine
Domain: Health Sciences
Open Access status: gold
Estimated APC paid: $1,200
OpenAlex ID: W4408522849
