ArticleCell death & disease2011
Treatment with a BH3 mimetic overcomes the resistance of latency III EBV (+) cells to p53-mediated apoptosis.
Article in Cell death & disease, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 17 citations in OpenAlex.
- The BCL-2 family protein inhibitor ABT-737 as an additional tool for the treatment of EBV-associated post-transplant lymphoproliferative disorders.Molecular oncology · 2020Article
- Raddeanin A promotes apoptosis and ameliorates 5-fluorouracil resistance in cholangiocarcinoma cells.World journal of gastroenterology · 2019Article
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- Developments in Burkitt's lymphoma: novel cooperations in oncogenic MYC signaling.Cancer management and research · 2014Review
- Molecular dynamics of the full-length p53 monomer.Cell cycle (Georgetown, Tex.) · 2013Article
- A threshold mechanism mediates p53 cell fate decision between growth arrest and apoptosis.Cell death and differentiation · 2013Article
- Epstein-Barr virus interactions with the Bcl-2 protein family and apoptosis in human tumor cells.Journal of Zhejiang University. Science. B · 2013Review
- The cellular ataxia telangiectasia-mutated kinase promotes epstein-barr virus lytic reactivation in response to multiple different types of lytic reactivation-inducing stimuli.Journal of virology · 2012Article
- Role of apoptosis in disease.Aging · 2012Review
- Analysis of apoptosis methods recently used in Cancer Research and Cell Death & Disease publications.Cell death & disease · 2012Article
- Cancer metabolism: current perspectives and future directions.Cell death & disease · 2012Review
- Article
- Epstein-Barr virus nuclear antigen 3C stabilizes Gemin3 to block p53-mediated apoptosis.PLoS pathogens · 2011Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
P53 inactivation is often observed in Burkitt's lymphoma (BL) cells due to mutations in the p53 gene or overexpression of its negative regulator, murine double minute-2 (MDM2). This event is now considered an essential part of the oncogenic process. Epstein-Barr virus (EBV) is strongly associated with BL and is a cofactor in its development. We previously showed that nutlin-3, an antagonist of MDM2, activates the p53 pathway in BL cell lines harboring wild-type p53. However, nutlin-3 strongly induced apoptosis in EBV (-) or latency I EBV (+) cells, whereas latency III EBV (+) cells were much more resistant. We show here that this resistance to apoptosis is also observed in latency III EBV (+) lymphoblastoid cell lines. We also show that, in latency III EBV (+) cells, B-cell lymphona 2 (Bcl-2) is selectively overproduced and interacts with Bcl-2-associated X protein (Bax), preventing its activation. The treatment of these cells with the Bcl-2-homology domain 3 mimetic ABT-737 disrupts Bax/Bcl-2 interaction and allows Bax activation by nutlin-3. Furthermore, treatment with these two compounds strongly induces apoptosis. Thus, a combination of Mdm2 and Bcl-2 inhibitors might be a useful anti-cancer strategy for diseases linked to EBV infection.
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