Viral driven epigenetic events alter the expression of cancer-related genes in Epstein-Barr-virus naturally infected Burkitt lymphoma cell lines

Abstract Epstein-Barr virus (EBV) was identified as the first human virus to be associated with a human malignancy, Burkitt’s lymphoma (BL), a pediatric cancer endemic in sub-Saharan Africa. The exact mechanism of how EBV contributes to the process of lymphomagenesis is not fully understood. Recent...

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Autores principales: Hector Hernandez-Vargas, Henri Gruffat, Marie Pierre Cros, Audrey Diederichs, Cécilia Sirand, Romina C. Vargas-Ayala, Antonin Jay, Geoffroy Durand, Florence Le Calvez-Kelm, Zdenko Herceg, Evelyne Manet, Christopher P. Wild, Massimo Tommasino, Rosita Accardi
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Publicado: Nature Portfolio 2017
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spelling oai:doaj.org-article:cf771775f0f0480bba14d8ec7e78bb0a2021-12-02T11:53:05ZViral driven epigenetic events alter the expression of cancer-related genes in Epstein-Barr-virus naturally infected Burkitt lymphoma cell lines10.1038/s41598-017-05713-22045-2322https://doaj.org/article/cf771775f0f0480bba14d8ec7e78bb0a2017-07-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-05713-2https://doaj.org/toc/2045-2322Abstract Epstein-Barr virus (EBV) was identified as the first human virus to be associated with a human malignancy, Burkitt’s lymphoma (BL), a pediatric cancer endemic in sub-Saharan Africa. The exact mechanism of how EBV contributes to the process of lymphomagenesis is not fully understood. Recent studies have highlighted a genetic difference between endemic (EBV+) and sporadic (EBV−) BL, with the endemic variant showing a lower somatic mutation load, which suggests the involvement of an alternative virally-driven process of transformation in the pathogenesis of endemic BL. We tested the hypothesis that a global change in DNA methylation may be induced by infection with EBV, possibly thereby accounting for the lower mutation load observed in endemic BL. Our comparative analysis of the methylation profiles of a panel of BL derived cell lines, naturally infected or not with EBV, revealed that the presence of the virus is associated with a specific pattern of DNA methylation resulting in altered expression of cellular genes with a known or potential role in lymphomagenesis. These included ID3, a gene often found to be mutated in sporadic BL. In summary this study provides evidence that EBV may contribute to the pathogenesis of BL through an epigenetic mechanism.Hector Hernandez-VargasHenri GruffatMarie Pierre CrosAudrey DiederichsCécilia SirandRomina C. Vargas-AyalaAntonin JayGeoffroy DurandFlorence Le Calvez-KelmZdenko HercegEvelyne ManetChristopher P. WildMassimo TommasinoRosita AccardiNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-17 (2017)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Hector Hernandez-Vargas
Henri Gruffat
Marie Pierre Cros
Audrey Diederichs
Cécilia Sirand
Romina C. Vargas-Ayala
Antonin Jay
Geoffroy Durand
Florence Le Calvez-Kelm
Zdenko Herceg
Evelyne Manet
Christopher P. Wild
Massimo Tommasino
Rosita Accardi
Viral driven epigenetic events alter the expression of cancer-related genes in Epstein-Barr-virus naturally infected Burkitt lymphoma cell lines
description Abstract Epstein-Barr virus (EBV) was identified as the first human virus to be associated with a human malignancy, Burkitt’s lymphoma (BL), a pediatric cancer endemic in sub-Saharan Africa. The exact mechanism of how EBV contributes to the process of lymphomagenesis is not fully understood. Recent studies have highlighted a genetic difference between endemic (EBV+) and sporadic (EBV−) BL, with the endemic variant showing a lower somatic mutation load, which suggests the involvement of an alternative virally-driven process of transformation in the pathogenesis of endemic BL. We tested the hypothesis that a global change in DNA methylation may be induced by infection with EBV, possibly thereby accounting for the lower mutation load observed in endemic BL. Our comparative analysis of the methylation profiles of a panel of BL derived cell lines, naturally infected or not with EBV, revealed that the presence of the virus is associated with a specific pattern of DNA methylation resulting in altered expression of cellular genes with a known or potential role in lymphomagenesis. These included ID3, a gene often found to be mutated in sporadic BL. In summary this study provides evidence that EBV may contribute to the pathogenesis of BL through an epigenetic mechanism.
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author Hector Hernandez-Vargas
Henri Gruffat
Marie Pierre Cros
Audrey Diederichs
Cécilia Sirand
Romina C. Vargas-Ayala
Antonin Jay
Geoffroy Durand
Florence Le Calvez-Kelm
Zdenko Herceg
Evelyne Manet
Christopher P. Wild
Massimo Tommasino
Rosita Accardi
author_facet Hector Hernandez-Vargas
Henri Gruffat
Marie Pierre Cros
Audrey Diederichs
Cécilia Sirand
Romina C. Vargas-Ayala
Antonin Jay
Geoffroy Durand
Florence Le Calvez-Kelm
Zdenko Herceg
Evelyne Manet
Christopher P. Wild
Massimo Tommasino
Rosita Accardi
author_sort Hector Hernandez-Vargas
title Viral driven epigenetic events alter the expression of cancer-related genes in Epstein-Barr-virus naturally infected Burkitt lymphoma cell lines
title_short Viral driven epigenetic events alter the expression of cancer-related genes in Epstein-Barr-virus naturally infected Burkitt lymphoma cell lines
title_full Viral driven epigenetic events alter the expression of cancer-related genes in Epstein-Barr-virus naturally infected Burkitt lymphoma cell lines
title_fullStr Viral driven epigenetic events alter the expression of cancer-related genes in Epstein-Barr-virus naturally infected Burkitt lymphoma cell lines
title_full_unstemmed Viral driven epigenetic events alter the expression of cancer-related genes in Epstein-Barr-virus naturally infected Burkitt lymphoma cell lines
title_sort viral driven epigenetic events alter the expression of cancer-related genes in epstein-barr-virus naturally infected burkitt lymphoma cell lines
publisher Nature Portfolio
publishDate 2017
url https://doaj.org/article/cf771775f0f0480bba14d8ec7e78bb0a
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