Quercetin Interrupts the Positive Feedback Loop Between STAT3 and IL-6, Promotes Autophagy, and Reduces ROS, Preventing EBV-Driven B Cell Immortalization

Biomolecules

Claudia Zompetta¹  MariaAnele Romeo¹  Mara Cirone¹  MariaSaveria Gilardini Montani¹  Alberto Faggioni¹  Roberta Santarelli¹  Roberta Gonnella¹  Marisa Granato¹  Gabriella D’Orazi² 

[1] Department of Experimental Medicine, “Sapienza” University of Rome, Laboratory affiliated to Istituto Pasteur Italia-Fondazione Cenci Bolognetti, 00161 Rome, Italy;Translational Research Area, Regina Elena National Cancer Institute, 00128 Rome, Italy;

关键词: quercetin;    Epstein–Barr virus (EBV), STAT3;    IL-6;    LCLs;    autophagy;    SQSTM1/p62;    ROS;   

DOI  :  10.3390/biom9090482

来源: DOAJ

【 摘 要 】

The oncogenic gammaherpesvirus Epstein−Barr virus (EBV) immortalizes in vitro B lymphocytes into lymphoblastoid cell lines (LCLs), a model that gives the opportunity to explore the molecular mechanisms driving viral tumorigenesis. In this study, we addressed the potential of quercetin, a widely distributed flavonoid displaying antioxidant, anti-inflammatory, and anti-cancer properties, in preventing EBV-driven B cell immortalization. The results obtained indicated that quercetin inhibited thectivation of signal transducer and activator of transcription 3 (STAT3) induced by EBV infection and reduced molecules such as interleukin-6 (IL-6) and reactive oxidative species (ROS) known to be essential for the immortalization process. Moreover, we found that quercetin promoted autophagy and counteracted the accumulation of sequestosome1/p62 (SQSTM1/p62), ultimately leading to the prevention of B cell immortalization. These findings suggest that quercetin may have the potential to be used to counteract EBV-driven lymphomagenesis, especially if its stability is improved.

【 授权许可】

Unknown