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• W2009389039 abstract "Background and Aims: Recent studies have shown epsterin-Barr virus (EBV) infection is related to the development of gastric cancer. In particular, latent EBV infection usually established persistently and promoted tumor progression. The zinc finger E-box binding factor 1 (ZEB1) mediated transcriptional silencing of intermediate-early genes and induced EBV infection from lytic to latent stage. We aim to study the effect of ZEB1 on modulating latent-lytic switch in gastric cancer, and to explore the potential of ZEB1 as a novel molecular target for the intervention of EBV associated Gastric Cancer (EBVaGc). Method Gastric cancer cell-lines with latent (YCC10 cell-line) and lytic (AGS-EBV infected cell-line) EBV infection were used in this study. Loss or gain function of ZEB1 was obtained by ZEB1 siRNA knockdown or forced re-expression experiments, respectively. The modulation of the intermediateearly gene and apoptotic mediators were assessed by real time RT-PCR and Western blot. Cell growth was evaluated by cell viability assay and colony formation assay, and cell cycle by flow cytometry analysis. Results: siRNA-mediated knockdown of ZEB1 in latent EBV infected cell-line YCC10 triggered a 3-fold enhanced expression of BZLF1, an intermediateearly gene of EBV, but a 5-fold reduction in expression of EBV nuclear antigen 1 (EBNA1), a gene that plays essential roles in enabling the replication and persistence of EBV genomes in latently infected cells and activating EBV latent gene expression. By doing so, knockdown of ZEB1 in YCC10 significantly inhibited cell viability (100% to 84%, P<0.01), suppressed cell proliferation as evidenced by reduced S phase cells (P=0.005), caused cell cycle arrest in G2M phase (P=0.006) and induced cell apoptosis (4.6±0.15% to 7.1±1.36%, P<0.05), The induction of cell apoptosis is confirmed by the cleavage of caspase-3 and PARP. On the other hand, over-expression of ZEB1 in lytic EBV infected cell line AGS-EBV through transient transfection significantly increased cell viability (P<0.01), induced S phase cell number (32.9±1.17% to 40.3±23.89%, P<0.05) and promoted colony formation (P<0.01). Conclusion: ZEB1 is involved in the latent-lytic switch of EBV associated gastric cancer. Inhibition of ZEB1 may be a promising approach for the treatment of EBVaGc." @default.
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• W2009389039 date "2010-05-01" @default.
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• W2009389039 title "M1912 Role of Zinc Finger E-Box Binding Factor 1 Modulating Latent-Lytic Switch of Epstein-Barr Virus in Gastric Cancer" @default.
• W2009389039 doi "https://doi.org/10.1016/s0016-5085(10)62023-9" @default.
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