期刊
FRONTIERS IN BIOSCIENCE-LANDMARK
卷 7, 期 -, 页码 D704-D716出版社
FRONTIERS IN BIOSCIENCE INC
DOI: 10.2741/subraman
关键词
Epstein Barr nuclear antigen; transcription; metastasis; cell cycle; Nm23-H1; prothymosin alpha; p300; review
资金
- NATIONAL CANCER INSTITUTE [R01CA091792, R01CA072150, R29CA072150] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DENTAL &CRANIOFACIAL RESEARCH [R01DE014136] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [T32GM007863] Funding Source: NIH RePORTER
- NCI NIH HHS [CA072150-01, CA91792-01] Funding Source: Medline
- NIDCR NIH HHS [DE14136-01] Funding Source: Medline
- NIGMS NIH HHS [T32 GM07863] Funding Source: Medline
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-Jkappa and HDAC1 modulates transcriptional activation. Additionally, EBNA3C disrupts the cyclin/cdk-Rb-E2F pathway that regulates cell cycle progression through the restriction point at G(1). Recent studies showed that the carboxy terminal region of EBNA3C from aa 366-992, essential for the immortalization of primary B-cells, interacts with Prothymosin (ProTalpha) and Nm23-H1. The interaction of EBNA3C with ProTalpha 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.
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