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

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• 作者：Sushil Kumar Sahu ; Suchitra Mohanty ; Amit Kumar ; Chanakya N. Kundu ; Subhash C. Verma ; Tathagata Choudhuri
• 关键词：EBNA3C ; Doxorubicin ; p73 ; 螖Np73 ; B-cell lymphoma ; EBV
• 刊名：Virology
• 出版年：5 January, 2014
• 年：2014
• 卷：448
• 期：Complete
• 页码：333-343
• 全文大小：3614 K

文摘

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 (螖Np73). 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 low螖Np73 level promotes the p73-mediated intrinsic pathway of apoptosis. In this report, we investigated the mechanism by which EBV infection counters p73伪-induced apoptosis through EBNA3C.