EBV Conference 2008 Guangzhou - Baylor College of Medicine

114 (RegID: 1917; 1918; 1919; 1920)
Qinyan Yin
Institution: Tulane University Health Sciences Center
e-mail: qyin@tulane.edu
MICRORNA 155 REGULATION IN EBV POSITIVE LYMPHOMA CELL
Qinyan Yin, Xia Wang, Jane McBride, Claire Fewell & Erik K. Flemington
Posterabstract:
MicroRNAs are a class of small non-coding RNAs that play a role in the regulation of cellular signaling
and developmental processes. A number of microRNAs have been shown to be either oncogenes or
tumor suppressors. One of the most highly implicated oncogenic microRNAs is miR-155. In
lymphocytes, miR-155 is induced by B cell receptor (BCR) engagement and we have previously shown
that induction of miR-155 by BCR activation is mediated by the transcription factors, JunB and FosB
which bind to a conserved AP-1 element in the miR-155 promoter. miR-155 is highly expressed in EBV
infected cells exhibiting type III latency but not type I latency and here we show that 1) miR-155
expression is induced by infection of EBV negative cells and by 5-Aza C induced expression of type III
latency genes in type I latency cells. 2) Inhibition of the ERK, JNK, or p38 pathways is not sufficient to
block miR-155 expression whereas inhibition of NF-kB suppresses expression of miR-155 and AP-1
proteins in the type III latency cell lines, IB4 and X50-7. 3) EMSA and ChIP analysis shows that the AP-1
proteins JunB, JunD and ATF3 bind to the miR-155 promoter and activate miR-155 in EBV positive type
III latency cells. 4) Reporter experiments and RT-PCR analysis of type I latency cells transduced with
retroviruses expressing latency gene products indicate a role of LMP1 and LMP2A in the induction of
miR-155. Nevertheless, our data indicate that LMP1 and LMP2A are insufficient to cause the high level
expression of miR-155 that is typically observed in type III latency cells. In summary, AP-1 proteins
induced by type III latency gene expression bind to the miR-155 promoter to regulate miR-155 expression
in type III latency cells.
EBV Conference 2008 Guangzhou
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