HBV Infection-Related Plays an Oncogenic Role by Regulating the PI3K-Akt Pathway and Fatty Acid Metabolism and Enhances Immunosuppression.

METHODS

We compared differentially expressed genes (DGEs) in HBV-positive and -negative tumor samples and conducted a Spearman correlation study between the DGEs and HBV titers within The Cancer Genome Atlas (TCGA). Moreover, we validated the results of our in-house samples.

RESULTS

In this study, we discovered a series of genes that correlated statistically with HBV infection based on the TCGA database. These genes were related to increased inflammation and some oncogenic signaling pathways via Gene Set Enrichment Analysis (GSEA). is an ideal gene, which mostly relates positively to HBV infection; moreover, it is overexpressed in human HCC, especially in those HBV-infected HCCs. After analyzing the TCGA data and performing a verification study using our own samples, expression was investigated to be significantly associated with PI3K-Akt signaling and fatty acid metabolism. Further, single-sample GSEA analysis of tumor immune cell infiltration gene sets revealed that high expression in HCC tissues was significantly associated with increased tumor-associated macrophages (TAMs) and regulatory T cells(Tregs).

CONCLUSIONS

is an HBV infection-related gene, which plays oncogenic roles, possibly due to enhancing PI3K-Akt, fatty acid usage in tumor cells and TAMs, and Treg-induced immunosuppression.