Functional interaction of Ugene and EBV infection mediates tumorigenic effects

摘要: Epstein–Barr virus (EBV) infection is associated with many human neoplasms, in which EBV-derived latent membrane protein-1 (LMP1) appears to be critical, but its exact oncogenic mechanism remains defined. To this end, our initial microarray analyses identified a LMP1-inducible gene, Ugene, originally characterized as binding partner for uracil DNA glycosylase 2, highly expressed malignant colon cancer. In report, it was found that designated herein LMP1-induced protein (LMPIP), induced, time-dependent manner, EBV-infected peripheral blood mononuclear cells and LMP1-transfected 293 cells. Functionally, when compared mock-transfected cells, overexpression of LMPIP nasopharyngeal carcinoma (NPC) cell lines resulted decrease reactive oxygen species production maintained mitochondria potential (Δψ) loss induced by H2O2. The NPC transfected also showed G1 population an increase the sub-G1 multiploid phase, concomitant increased levels cycle activators, including cyclin D1 CDK4. contrast, silencing expression tumor short hairpin RNA interference revealed significantly decreased at G1/S while number phase increased. Significantly, knock-down tumorigenic transforming activity ectopic LMP1 expression, determined soft agar foci size nude mice. Further, elevated noted cytoplasm nuclei mass non-EBV-infected lines. These results suggested may have important mediator role EBV-mediated neoplasm serve new target therapy tumors EBV infection.