IMR Press / FBL / Volume 7 / Issue 4 / DOI: 10.2741/subraman

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience.

Article
The Epstein Barr nuclear antigen EBNA3C regulates transcription, cell transformation and cell migration
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1 Department of Microbiology and Immunology and Cell and Molecular Biology Graduate Program, University of Michigan Medical School, Ann Arbor, MI, USA
Front. Biosci. (Landmark Ed) 2002, 7(4), 704–716; https://doi.org/10.2741/subraman
Published: 1 March 2002
Abstract

The Epstein-Barr virus (EBV) infects most of the human population and persists in B-lymphocytes for the lifetime of the host. During the establishment of latent infection a unique repertoire of genes are expressed. The EBV nuclear antigen EBNA3C is essential for growth transformation of primary B-lymphocytes in vitro. EBNA3C regulates the transcription of a number of viral and cellular genes important for the immortalization process. Interaction of EBNA3C with the cellular transcription factor RBP-Jκ and HDAC1 modulates transcriptional activation. Additionally, EBNA3C disrupts the cyclin/cdk-Rb-E2F pathway that regulates cell cycle progression through the restriction point at G1. Recent studies showed that the carboxy terminal region of EBNA3C from aa 366-992, essential for the immortalization of primary B-cells, interacts with Prothymosinα (ProTα) and Nm23-H1. The interaction of EBNA3C with ProTα as well as the histone acetylase p300 suggested a possible role in modulation of histone acetylation and chromatin remodeling. Cell migration assays geared towards determining the effect of EBNA3C on Nm23-H1 antimetastatic function suggests that EBNA3C suppresses the effects of NM23-H1 on the motility of breast carcinoma as well as Burkitt's lymphoma cells. This observation suggests that EBNA3C may be involved in driving the metastatic process in EBV associated human malignancies.

Keywords
Epstein Barr Nuclear Antigen
transcription
metastasis
cell cycle
Nm23-H1
Prothymosin a
p300
Review
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