HepG2 Attenuation Induced by RNase A Modulates Gene Profiling and Immunophenotypic Characterization of Some Immune Cells Operating in Cancer Vaccine

Abstract

Hepatocellular carcinoma (HCC) ranks as the third leading cause of cancer death. Attempts to induce an effective immune response against cancer by immunotherapeutic intervention, including activation of dendritic cells (DCs), were established. The present study was undertaken to investigate the attenuation of HepG2 cells using ribonuclease enzyme A (RNase A) as a possible biological factor to sensitize allogenic DCs and lymphocytes isolated from Egyptian HCC patients. Attenuation of HepG2 cells resulted in a significant increase in activated DC and T-lymphocyte markers, upregulation of CD44 gene expression and increased lactate dehydrogenase as well as interleukin-12 levels. In contrast, a significant decrease in matureDCs, B-cells, T-helper, cytotoxic T-cells, and NK-cells, as well as LMP-2 gene expression was recorded. In conclusion, the attenuation of HepG2 cells with RNase A and subsequent pulsation to allogenic DCs and lymphocytes caused a differential immune response. Further studies are recommended to explain the role of RNase A in modulating antigen expression on the tumor cell surface.