Hong Kong Med J 2013;19(Suppl 5):S39-42
Latent-lytic switch of Epstein-Barr virus infection in gastric carcinoma
J Yu, HC Jin
Institute of Digestive Disease, Prince of Wales Hospital, The Chinese University of Hong Kong
1. Epstein-Barr virus (EBV) causes gastric cancer and was almost always latent in infected tumour cells. Tumour cells infected with the latent stage of EBV do not respond to the antiviral drug ganciclovir. Zinc finger E-box binding factor (ZEB1) is the transcriptional repressor pivotal for silencing the BZLF1 promoter (Zp). BZLF1 is sufficient to convert EBV from the latent to lytic form. However, the mechanism of ZEB1 regulating latent-lytic switch of the EBV life cycle in EBV-associated gastric cancer and the virus’s role in gastric carcinogenesis remain unknown.
2. We investigated the effect of ZEB1 on latent-lytic switch of EBV infection in gastric cancer cell lines. Loss or gain of ZEB1 biological function indicated its potential as a novel molecular target for the intervention in EBV-associated gastric cancer.
3. In addition, TaqMan real-time PCR was performed to examine the existence of EBV in primary gastric cancer and premalignant lesions. The association between EBV and patient characteristics was assessed.
4. Our results suggest that ZEB1 is a key mediator of the latent-lytic switch of EBV-associated gastric cancer. Inhibition of ZEB1 may be a potential means of therapy.