Cooperative interactions among p53, bcl-2 and Epstein-Barr virus latent membrane protein 1 in nasopharyngeal carcinoma cells

Interactions among p53, bcl‐2 and Epstein–Barr virus (EBV) latent membrane protein 1 (LMP1) in nasopharyngeal carcinoma (NPC) cells were evaluated by gene cotransfections. The data showed that bcl‐2 expression was not only able to prevent the growth suppression induced by wild‐type p53 but was also paradoxically able to inhibit the growth enhancement induced by mutant p53. Latent membrane protein 1 was shown to be capable of overcoming the growth inhibition induced by wild‐type p53 and the synergistic cooperation with bcl‐2 to enhance cellular growth. Latent membrane protein 1 could also cooperate with mutant p53 to provide a growth advantage for NPC cells. Most NPC revealed detectable overexpression of p53, and the majority of those were a wild type possibly responding to EBV infection. The coexpression of bcl‐2 and LMP1 was thought to inhibit the growth suppression induced by wild‐type p53 in NPC. But there was no associated expression between LMP1 and bcl‐2 because we demonstrated that transfected LMP1 failed to induce bcl‐2 expression in NPC cells in contrast to the findings in B cells. It is theorized that the cooperative expression of bcl‐2 and LMP1 exists in the majority of NPC, while a minority of NPC have cooperative expression of LMP1 and mutant p53. Each cooperative interaction could play an important role in the development and progression of NPC.