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EBV interferes with the sensitivity of Burkitt lymphoma Akata cells to etoposide.

Abstract
Burkitt lymphoma (BL) commonly exhibits Epstein-Barr virus (EBV) positivity associated with latent chronic infection. Models of acute EBV infection have been associated with cellular resistance to apoptosis. However, the effect of latent long-term EBV infection on apoptosis induced by drugs is not well defined. To determine this, we have studied the response of the Akata EBV+ cell line (type I latency) to etoposide, before and after downregulating EBV gene expression. We observed that downregulating EBV nuclear antigen-1 (EBNA-1) expression with siRNAs reverted cellular sensitivity to etoposide. In accordance with this finding, Akata EBV+ cells showed increased sensitivity to etoposide, when compared to the Akata EBV- cells. We also observed that Akata EBV+ cells presented increased apoptosis levels and decreased Bcl-xL mRNA and protein levels, when compared to the Akata EBV- cells. In addition, Akata EBV+ cells contained less endoplasmic reticulum (ER) than EBV- cells. Finally, downregulation of EBV with EBNA-1 siRNAs caused an increase in the expression of Bcl-xL indicating that EBV is responsible for the differences found between the Akata EBV+ and EBV- cell lines.
AuthorsRaquel T Lima, Hugo Seca, Paula Soares, Maria São José Nascimento, M Helena Vasconcelos
JournalJournal of cellular biochemistry (J Cell Biochem) Vol. 112 Issue 1 Pg. 200-10 (Jan 2011) ISSN: 1097-4644 [Electronic] United States
PMID21069730 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Antineoplastic Agents, Phytogenic
  • Epstein-Barr Virus Nuclear Antigens
  • RNA, Messenger
  • RNA, Small Interfering
  • Viral Matrix Proteins
  • bcl-X Protein
  • Etoposide
  • EBV-encoded nuclear antigen 1
Topics
  • Antineoplastic Agents, Phytogenic (pharmacology)
  • Apoptosis
  • Burkitt Lymphoma (virology)
  • Cell Line, Tumor
  • Down-Regulation
  • Epstein-Barr Virus Nuclear Antigens (genetics, metabolism)
  • Etoposide (pharmacology)
  • Herpesvirus 4, Human (pathogenicity)
  • Humans
  • RNA, Messenger (metabolism)
  • RNA, Small Interfering (metabolism)
  • Viral Matrix Proteins (genetics, metabolism)
  • bcl-X Protein (genetics, metabolism)

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