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KSHV LANA and EBV LMP1 induce the expression of UCH-L1 following viral transformation.

Abstract：

:Ubiquitin C-terminal Hydrolase L1 (UCH-L1) has oncogenic properties and is highly expressed during malignancies. We recently documented that Epstein-Barr virus (EBV) infection induces uch-l1 expression. Here we show that Kaposi's Sarcoma-associated herpesvirus (KSHV) infection induced UCH-L1 expression, via cooperation of KSHV Latency-Associated Nuclear Antigen (LANA) and RBP-Jκ and activation of the uch-l1 promoter. UCH-L1 expression was also increased in Primary Effusion Lymphoma (PEL) cells co-infected with KSHV and EBV compared with PEL cells infected only with KSHV, suggesting EBV augments the effect of LANA on uch-l1. EBV latent membrane protein 1 (LMP1) is one of the few EBV products expressed in PEL cells. Results showed that LMP1 was sufficient to induce uch-l1 expression, and co-expression of LMP1 and LANA had an additive effect on uch-l1 expression. These results indicate that viral latency products of both human γ-herpesviruses contribute to uch-l1 expression, which may contribute to the progression of lymphoid malignancies.

journal_name

Virology

journal_title

Virology

authors

Bentz GL,Bheda-Malge A,Wang L,Shackelford J,Damania B,Pagano JS

doi

10.1016/j.virol.2013.10.018

subject

Has Abstract

pub_date

2014-01-05 00:00:00

pages

293-302

eissn

0042-6822

issn

1096-0341

pii

S0042-6822(13)00578-3

journal_volume

448

pub_type

杂志文章

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