(-)-Epigallocatechin‑3‑gallate inhibition of Epstein‑Barr virus spontaneous lytic infection involves downregulation of latent membrane protein 1
- Sufang Liu
- Hongde Li
- Min Tang
- Ya Cao
Published online on: November 13, 2017
The Epstein‑Barr virus (EBV) lytic cycle contributes to the development of EBV‑associated diseases. EBV‑encoded latent membrane protein 1 (LMP1) is key to EBV lytic replication, and our previous work indicated that epigallocatechin‑3‑gallate (EGCG) inhibited constitutive EBV lytic infection through the suppression of LMP1‑activated phosphoinositide 3‑kinase/Akt and mitogen‑activated protein kinase kinase/extracellular signal‑related protein kinase 1/2 signaling. The present study demonstrated that LMP1 in CNE‑LMP1 constructed cells significantly induced the expression of the EBV lytic proteins BZLF1 (P<0.001) and BMRF1 (P<0.05) compared with CNE1 cells. Following treatment with a specific DNAzyme that targets LMP1, significantly reduced protein expression levels of BZLF1 and BMRF1 in EBV‑associated epithelial carcinoma CNE1‑LMP1 cells (P<0.001 and P<0.01, respectively) and lymphoma B95.8 cells (both P<0.01) were observed. Furthermore, EGCG significantly inhibited the mRNA and protein expression levels of LMP1 (P<0.05) in an apparent dose‑dependent manner in CNE1‑LMP1 and B95.8 cells. Thus, the present findings indicated that the molecular mechanism underlying EGCG inhibition of EBV lytic infection involves downregulation of LMP1.