Abstract
Epstein-Barr virus nuclear antigen 1 (EBNA1) is associated with the pathogenesis of Epstein-Barr virus-associated gastric carcinoma (EBVaGC). However, the function of EBNA1 in the growth of EBVaGC cells remains unclear. In the present study, the effects of silencing EBNA1, by RNA interference (RNAi), on the growth of EBVaGC cells were investigated in vitro and in vivo. A lentivirus-mediated RNAi targeting EBNA1 was transfected into the EBVaGC cell line GT-38. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR), western blot analysis, MTT, colony formation and flow cytometry were performed to evaluate the biological behavior of GT-38 cells that were transfected with EBNA1 small interfering RNA (siRNA) in vitro. The effects of silencing EBNA1 on tumor growth were assessed in a tumor xenograft model using BALB/c nude mice. The results demonstrated that the proliferative and clonogenic abilities of GT-38 cells were significantly downregulated in response to EBNA1 siRNA (P<0.01). Furthermore, EBNA1 siRNA induced cell cycle arrest in the G0/G1 phase and promoted apoptosis of GT-38 cells (P<0.01). The tumorigenicity of GT-38 cells was significantly inhibited in the EBNA1 siRNA group. The results revealed that lentivirus-mediated RNAi of EBNA1 inhibited the growth of the EBVaGC cell line GT-38 in vitro and in vivo. Therefore, EBNA1 may be a potential target for gene therapy in EBVaGC.