Effect of abnormal oligonucleotide binding folding domain protein gene on the initiation of DNA replication in hepatocellular carcinoma / 医学研究生学报

ABSTRACT

ObjectiveThere are few reports about abnormal oligonucleotide binding fold domain protein genes (OBGs) affecting the initiation of DNA replication in hepatocellular carcinoma through the microchromosome maintenance (MCM) complex. This study aims to explore the roles of reverse-transcription-related genes (RTGs) in Hepatocellular Carcinoma cells (HCC) and the correlation between gene polymorphisms and abnormal gene expression.Methods We created a mouse model by injecting hepatocellular carcinoma cell line H22 (logarithmic growth phase) and dissected the tumor bodies from tumor-forming mice. The control group was treated by isotonic saline without H22. The healthy liver tissue cells were taken from the control mice. The total RNA of the H22 group and control group were extracted, and differentially expressed genes were analyzed. Screening of differentially expressed reverse transcription-related DEGs (RDEGs), GO and KEGG analysis of RDEGs. The interaction analysis of RDEGs encoded proteins, and the correlation analysis of RDEGs polymorphism and gene expression.ResultsThere were 193 differentially expressed RTGs in HCCs, which were involved in two biological procedures, three cell components, one molecular function, three signal pathways, and three functional sites; Its function is mainly concentrated in DNA replication, especially the construction of MCM complex and telomere complex in which OBGs participate in the initiation of replication. Most related genes had OB fold domains. The results also showed that both AS and SNV caused gene polymorphism was positively correlated with gene expression, and most OBGs in HCC had SNV phenomenon, but not occurred in healthy liver tissue.Conclusion Collectively, AS and SNV may be important regulatory factors for gene expression. SNV may particularly affect the function of OBGs in the MCM complex to abnormally initiate DNA replication in HCC.