Epstein-barr virus regulates c-MYC, apoptosis, and tumorigenicity in Burkitt lymphoma.

摘要: Loss of the Epstein-Barr virus (EBV) genome from Akata Burkitt lymphoma (BL) cells is coincident with a loss malignant phenotype, despite fact that and other EBV-positive BL express restricted set EBV gene products (type I latency) are not known to overtly affect cell growth. Here we demonstrate reestablishment type latency in EBV-negative restores tumorigenicity tumorigenic potential correlates an increased resistance apoptosis under growth-limiting conditions. The antiapoptotic effect was associated higher level Bcl-2 expression EBV-dependent decrease steady-state levels c-MYC protein. Although EBNA-1 protein expressed all EBV-associated tumors reported have oncogenic potential, enforced alone failed restore or down-regulation c-MYC. These data provide direct evidence contributes suggest novel model whereby program promotes B-cell survival, thus persistence within immune host, by selectively targeting