EBV latent membrane protein 2A orchestrates p27^kip1 degradation via Cks1 to accelerate MYC-driven lymphoma in mice.

ABSTRACT: Epstein-Barr virus (EBV) establishes lifelong infection in B lymphocytes of most human hosts and is associated with several B lymphomas. During latent infection, EBV encodes latent membrane protein 2A (LMP2A) to promote the survival of B cells by mimicking host B-cell receptor signaling. By studying the roles of LMP2A during lymphoma development in vivo, we found that LMP2A mediates rapid MYC-driven lymphoma onset by allowing B cells to bypass MYC-induced apoptosis mediated by the p53 pathway in our transgenic mouse model. However, the mechanisms used by LMP2A to facilitate transformation remain elusive. In this study, we demonstrate a key role of LMP2A in promoting hyperproliferation of B cells by enhancing MYC expression and MYC-dependent degradation of the p27^kip1 tumor suppr

SUBMITTER: Fish K 

PROVIDER: S-EPMC5721284 | biostudies-literature | 2017 Dec

REPOSITORIES: biostudies-literature