Epigallocatechin-3-Gallate Suppresses Human Herpesvirus 8 Replication and Induces ROS Leading to Apoptosis and Autophagy in Primary Effusion Lymphoma Cells

Autor: Miao-Chen Chou, Chang-Yu Chen, Ching-Yi Tsai, Mei-Han Huang, Yee-Hsuan Chiou, Kuan-Hua Lin, Yi-Fen Wang, Huey-Wen Shyu
Jazyk: angličtina
Rok vydání: 2017
Předmět:
0301 basic medicine
Cell
Virus Replication
Catechin
lcsh:Chemistry
EGCG
primary effusion lymphoma
ROS
apoptosis
autophagy
lcsh:QH301-705.5
Spectroscopy
Chemistry
food and beverages
virus diseases
General Medicine
Herpesviridae Infections
Cell cycle
Computer Science Applications
medicine.anatomical_structure
Herpesvirus 8
Human
Primary effusion lymphoma
Programmed cell death
Cell Survival
Antineoplastic Agents
complex mixtures
Antiviral Agents
Catalysis
Article
Inorganic Chemistry
03 medical and health sciences
Cell Line
Tumor
Lymphoma
Primary Effusion
medicine
Humans
Viability assay
Physical and Theoretical Chemistry
Molecular Biology
Dose-Response Relationship
Drug
Organic Chemistry
Autophagy
medicine.disease
Molecular biology
030104 developmental biology
HEK293 Cells
lcsh:Biology (General)
lcsh:QD1-999
Apoptosis
Cancer cell
Reactive Oxygen Species
Zdroj: International Journal of Molecular Sciences
International Journal of Molecular Sciences; Volume 19; Issue 1; Pages: 16
International Journal of Molecular Sciences, Vol 19, Iss 1, p 16 (2017)
ISSN: 1422-0067
Popis: 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.
Databáze: OpenAIRE
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