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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&lt;0.01). Furthermore, EBNA1 siRNA induced cell cycle arrest in the G0/G1 phase and promoted apoptosis of GT-38 cells (P&lt;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.

Lentivirus‑mediated RNA interference targeting EBNA1 gene inhibits the growth of GT‑38 cells in�vitro and in�vivo