Epstein-Barr virus nuclear protein EBNA-3C interacts with the human metastatic suppressor Nm23-H1: A molecular link to cancer metastasis
Chitra Subramanian, Murray A. Cotter II
& Erle S. Robertson
Program in Cellular and Molecular Biology, Department of Microbiology and Immunology and the Comprehensive Cancer and Geriatrics Center, University of Michigan Medical School, Ann Arbor, Michigan, USA
Correspondence should be addressed to Erle S. Robertson esrobert@umich.edu
Epstein-Barr virus (EBV) is an oncogenic virus associated with a number of human malignancies including Burkitt lymphoma, nasopharyngeal carcinoma, lymphoproliferative disease and, though still debated, breast carcinoma. A subset of latent EBV antigens is required for mediating immortalization of primary B-lymphocytes. Here we demonstrate that the carboxy-terminal region of the essential latent antigen, EBNA-3C, interacts specifically with the human metastatic suppressor protein Nm23-H1. Moreover, EBNA-3C reverses the ability of Nm23-H1 to suppress the migration of Burkitt lymphoma cells and breast carcinoma cells. We propose that EBNA-3C contributes to EBV-associated human cancers by targeting and altering the role of the metastasis suppressor Nm23-H1.
