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EGCG debilitates the persistence of EBV latency by reducing the DNA binding potency of nuclear antigen 1.

Abstract：

:Because the expression of EBNA1 is prevalent in all EBV-associated tumors, it has become one of the most attractive drug targets for the discovery of anti-EBV compounds. In a cell-based reporter system, EBNA1 consistently upregulated the transcription of an oriP-Luc mini-EBV episome by 6- to 8-fold. The treatment of cells with 50 μM EGCG effectively blocked the binding of EBNA1 to oriP-DNA both in vivo and in vitro, which led to the abrogation of EBNA1-dependent episome maintenance and transcriptional enhancement. Importantly, the anti-EBNA1 effects caused by EGCG ultimately impaired the persistence of EBV latent infection. Our data suggest that the inhibition of EBNA1 activity by EGCG could be a promising starting point for the development of new protocols for anti-EBV therapy.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Chen YL,Tsai HL,Peng CW

doi

10.1016/j.bbrc.2011.12.104

subject

Has Abstract

pub_date

2012-01-20 00:00:00

pages

1093-9

issue

3

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(11)02313-8

journal_volume

417

pub_type

杂志文章

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