Abstract
Epigallocatechin-3-gallate (EGCG), the major constituent of green tea, has been shown to induce cell death in cancer cells. Primary effusion lymphoma (PEL) is an aggressive neoplasm caused by human herpesvirus 8 (HHV8). In this study, we examined the role of EGCG on PEL cells in cell death and HHV8 replication. We performed trypan blue exclusion assay to assess the cell viability of PEL cells, flow cytometry analysis to examine the cell cycle distribution and reactive oxygen species (ROS) generation, caspase-3 activity to assay apoptosis, acridine orange staining to determine autophagy, and immunoblotting to detect the protein levels involved in apoptosis and autophagy as well as mitogen activated protein kinases (MAPKs) activation upon EGCG treatment. The expression of the HHV8 lytic gene was determined by luciferase reporter assay and reverse transcription-PCR, and viral progeny production was determined by PCR. Results revealed that EGCG induced cell death and ROS generation in PEL cells in a dose-dependent manner. N-acetylcysteine (NAC) inhibited the EGCG-induced ROS and rescued the cell from EGCG-induced cell death. Even though EGCG induced ROS generation in PEL cells, it reduced the production of progeny virus from PEL cells without causing HHV8 reactivation. These results suggest that EGCG may represent a novel strategy for the treatment of HHV8 infection and HHV8-associated lymphomas.
Highlights
Primary effusion lymphoma (PEL) is caused by the clonal expansion of human herpesvirus 8 (HHV8; known as Kaposi’s sarcoma-associated herpesvirus)-infected B cells [1]
Our data demonstrate that EGCG induces cell death in PEL cells via a mechanism involving the generation of reactive oxygen species (ROS)
The cellular viability was assessed using trypan blue exclusion assay. Both HHV8 containing PEL cell lines were susceptible to EGCG in a dose-dependent manner (Figure 1A)
Summary
Primary effusion lymphoma (PEL) is caused by the clonal expansion of human herpesvirus 8 (HHV8; known as Kaposi’s sarcoma-associated herpesvirus)-infected B cells [1]. The effects of EGCG on PEL cells and HHV8 replication in PEL cells have not yet been reported. Our data demonstrate that EGCG induces cell death in PEL cells via a mechanism involving the generation of ROS. Even though EGCG induced ROS generation in PEL cells, it reduced the production of progeny virus from PEL cells without causing HHV8 reactivation. These results suggest that EGCG may represent a novel strategy for the treatment of HHV8 infection and HHV8-associated lymphomas
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