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Targeted Therapy for EBV-Associated B-cell Neoplasms.

Siddhartha Ganguly1,2, Sudhakiranmayi Kuravi1,2, Satyanarayana Alleboina1,2

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Ixazomib, an oral proteasome inhibitor, effectively inhibits growth and induces apoptosis in Epstein-Barr virus (EBV)-infected B-cell lines. This study supports ixazomib as a potential therapy for EBV-associated B-cell neoplasms by targeting the NF-κB pathway.

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Area of Science:

  • Oncology
  • Virology
  • Molecular Biology

Background:

  • Epstein-Barr virus (EBV) is linked to B-cell lymphoid malignancies.
  • NF-κB pathway activation is a hallmark of EBV-associated lymphomas.
  • The ubiquitin/proteasome system regulates the NF-κB pathway.

Purpose of the Study:

  • To evaluate ixazomib's preclinical efficacy against EBV-infected B-lymphoblastoid cell lines.
  • To investigate the effects of ixazomib on cell growth, apoptosis, and cell cycle.
  • To elucidate the molecular mechanisms underlying ixazomib's action in EBV-associated B-cells.

Main Methods:

  • Treatment of EBV-infected Raji and Daudi cell lines with ixazomib.
  • Assessment of cell viability, apoptosis, and cell-cycle progression.
  • Analysis of protein levels, including p53, p21, p27, survivin, c-Myc, IκBα, and p65.

Main Results:

  • Ixazomib induced dose-dependent apoptosis and G2-M cell-cycle arrest.
  • Ixazomib increased p53, p21, and p27 levels, while decreasing survivin and c-Myc.
  • Ixazomib treatment led to polyubiquitinated protein accumulation and reduced p65 nuclear translocation.

Conclusions:

  • Ixazomib demonstrates significant preclinical anti-proliferative and pro-apoptotic effects on EBV-infected B-cells.
  • Ixazomib targets the NF-κB pathway by inhibiting proteasome function.
  • These findings support further investigation of ixazomib for EBV-associated B-cell neoplasms.