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2018 ; 9
(12
): 10417-10435
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Epstein-Barr virus stably confers an invasive phenotype to epithelial cells
through reprogramming of the WNT pathway
#MMPMID29535816
Birdwell CE
; Prasai K
; Dykes S
; Jia Y
; Munroe TGC
; Bienkowska-Haba M
; Scott RS
Oncotarget
2018[Feb]; 9
(12
): 10417-10435
PMID29535816
show ga
Epstein-Barr virus (EBV)-associated carcinomas, such as nasopharyngeal carcinoma
(NPC), exhibit an undifferentiated and metastatic phenotype. To determine viral
contributions involved in the invasive phenotype of EBV-associated carcinomas,
EBV-infected human telomerase-immortalized normal oral keratinocytes (NOK) were
investigated. EBV-infected NOK were previously shown to undergo epigenetic
reprogramming involving CpG island hypermethylation and delayed responsiveness to
differentiation. Here, we show that EBV-infected NOK acquired an invasive
phenotype that was epigenetically retained after viral loss. The transcription
factor lymphoid enhancer factor 1 (LEF1) and the secreted ligand WNT5A, expressed
in NPC, were increased in EBV-infected NOK with sustained expression for more
than 20 passages after viral loss. Increased LEF1 levels involved four LEF1
variants, and EBV-infected NOK showed a lack of responsiveness to ?-catenin
activation. Although forced expression of WNT5A and LEF1 enhanced the
invasiveness of parental NOK, LEF1 knockdown reversed the invasive phenotype of
EBV-infected NOK in the presence of WNT5A. Viral reprogramming of LEF1 and WNT5A
was observed several passages after EBV infection, suggesting that LEF1 and WNT5A
may provide a selective advantage to virally-infected cells. Our findings suggest
that EBV epigenetically reprogrammed epithelial cells with features of basal,
wound healing keratinocytes, with LEF1 contributing to the metastatic phenotype
of EBV-associated carcinomas.
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