Elsevier

Virology

Volume 448, 5 January 2014, Pages 333-343
Virology

Epstein–Barr virus nuclear antigen 3C interact with p73: Interplay between a viral oncoprotein and cellular tumor suppressor

https://doi.org/10.1016/j.virol.2013.10.023Get rights and content
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Highlights

  • EBV-encoded EBNA3C suppresses doxorubicin-induced apoptosis in B-cell lymphomas.

  • EBNA3C binds to p73 to suppress its apoptotic effect.

  • EBNA3C maintains latency by regulating downstream mitochondrial pathways.

Abstract

The p73 protein has structural and functional homology with the tumor suppressor p53, which plays an important role in cell cycle regulation, apoptosis, and DNA repair. The p73 locus encodes both a tumor suppressor (TAp73) and a putative oncogene (ΔNp73). p73 May play a significant role in p53-deficient lymphomas infected with Epstein–Barr virus (EBV). EBV produces an asymptomatic infection in the majority of the global population, but it is associated with several human B-cell malignancies. The EBV-encoded Epstein–Barr virus nuclear antigen 3C (EBNA3C) is thought to disrupt the cell cycle checkpoint by interacting directly with p53 family proteins. Doxorubicin, a commonly used chemotherapeutic agent, induces apoptosis through p53 and p73 signaling such that the lowΔNp73 level promotes the p73-mediated intrinsic pathway of apoptosis. In this report, we investigated the mechanism by which EBV infection counters p73α-induced apoptosis through EBNA3C.

Keywords

EBNA3C
Doxorubicin
p73
ΔNp73
B-cell lymphoma
EBV

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