Cuproptosis is a new type of cell death that depends on intracellular copper accumulation to trigger the aggregation of mitochondrial lipoacylated protein and the degradation of iron-sulfur cluster protein,with a different mechanism of action from autophagy,ferroptosis,pyroptosis,and necroptosis.Cuproptosis is closely association with the development of liver cancer and resistance to antitumor drugs,as well as the progression of various liver diseases such as hereditary liver diseases,nonalcoholic fatty liver disease,viral hepatitis,and liver cirrhosis.This article summarizes the mechanism of cuproptosis and its role in liver diseases,in order to provide a reference for further research and treatment of liver diseases.

Objective: To construct the mutants of ARID1A gene, which is an important component in human chromosomal remodeling complex Switch/Sucrose Non Fermentable (SWI/SNF), and identify their overexpression in liver cancer HepG2 cells. Methods: Overlap PCR was used to construct domain truncated mutantss pcDNA6-ARID1A/ΔARID and pcDNA6-ARID1A/ΔD UF3518 based on wild type plasmids pcDNA6-ARID1A. Lipofectionmethod was used to transfect the wild type and mutants into HepG2. Real-time PCR and western blotting were used to confirm the overexpression of ARID1A and the mutants. Results: SDS-PAGE and sequencingresult confirmed the successful construction of pcDNA6-ARID1A/ΔARID and pcDNA6-ARID1A/ΔDUF3518. Real-time PCR and western blottingresult confirmed the overexpression of both mRNA and protein of wild type ARID1A and ARID1A/ΔARID. The mRNA levels indicated that ARID1A/Δ DUF3518 were overexpressed, but the protein levels were quite low. Conclusions Functional domain truncated mutants of ARID1A were successfully constructed. Overexpression of wild type ARID1A and ARID1A/ΔARID in liver cancer HepG2 cells was successful. Loss of ARID1A/ΔDUF3518 protein suggest that DUF3518 may contribute to the protein structure stability.