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Quercetin Interrupts the Positive Feedback Loop Between STAT3 and IL-6, Promotes Autophagy, and Reduces ROS,

Marisa Granato1, Maria Saveria Gilardini Montani2, Claudia Zompetta3

  • 1Department of Experimental Medicine, "Sapienza" University of Rome, Laboratory affiliated to Istituto Pasteur Italia-Fondazione Cenci Bolognetti, 00161 Rome, Italy. marisa.granato@uniroma1.it.

Biomolecules
|September 25, 2019
PubMed

Insights

Quercetin, an antioxidant flavonoid, prevents Epstein-Barr virus (EBV) from immortalizing B cells. It inhibits key signaling pathways and promotes cell death, offering potential for combating EBV-driven cancers.

Area of Science:

  • Oncology
  • Virology
  • Molecular Biology
  • Immunology

Background:

  • Epstein-Barr virus (EBV) is an oncogenic gammaherpesvirus that immortalizes B lymphocytes in vitro, creating lymphoblastoid cell lines (LCLs).
  • This EBV-driven B cell immortalization process is a crucial model for studying viral tumorigenesis.
  • Key molecular mechanisms, including STAT3 activation, IL-6, and ROS, are essential for this immortalization.

Purpose of the Study:

  • To investigate the potential of quercetin, a flavonoid with known antioxidant, anti-inflammatory, and anti-cancer properties, in preventing EBV-induced B cell immortalization.
  • To elucidate the molecular mechanisms by which quercetin might inhibit EBV-driven lymphomagenesis.

Main Methods:

  • In vitro study using EBV-infected B lymphocytes (LCLs).
  • Assessment of quercetin's effects on STAT3 activation, IL-6, ROS production, autophagy, and SQSTM1/p62 levels.
  • Evaluation of quercetin's impact on B cell immortalization.

Main Results:

  • Quercetin inhibited EBV-induced activation of signal transducer and activator of transcription 3 (STAT3).
  • Quercetin reduced levels of interleukin-6 (IL-6) and reactive oxidative species (ROS), which are critical for immortalization.
  • Quercetin promoted autophagy and counteracted the accumulation of sequestosome1/p62 (SQSTM1/p62), preventing B cell immortalization.

Conclusions:

  • Quercetin demonstrates potential in preventing EBV-driven B cell immortalization.
  • The anti-tumorigenic effects of quercetin involve the inhibition of STAT3 signaling, reduction of IL-6 and ROS, and modulation of autophagy.
  • Further research, particularly on improving quercetin's stability, is warranted to explore its therapeutic application against EBV-associated lymphomagenesis.
Keywords:
Epstein–Barr virus (EBV), STAT3IL-6LCLsROSSQSTM1/p62autophagyquercetin

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