Implications for new therapeutic targets for B cell lymphomas and other EBV-associated illnesses
Earlier this year, researchers at the University of Pennsylvania School of Medicine identified a link between a critical cancer pathway and an Epstein-Barr Virus (EBV) protein known to be expressed in a number of EBV-associated cancers. Their findings demonstrated a new mechanism by which EBV can transform human B cells from the immune system into cancerous cells, which can lead to B-cell lymphomas. Now, they have found that the viral protein--called EBNA3C (for EBV nuclear antigen)--mediates the degradation of the retinoblastoma protein, an important molecular brake for cell proliferation.
Erle S. Robertson, PhD, an Associate Professor of Microbiology who leads the Tumor Virology Program at Penns Abramson Cancer Center, and MD/PhD student Jason Knight, published their results last week in the Proceedings of the National Academy of Sciences.
The retinoblastoma protein (Rb) is a major regulator of several genes in charge of cell proliferation and cell-cycle regulation. In the nucleus, Rb normally binds to E2F, turning off genes involved with cell proliferation. Using human cell cultures infected with the Epstein-Barr virus, the investigators found that EBNA3C recruits a group of molecules called the SCF complex, which attaches ubiquitin to Rb. This inadvertently tags Rb for degradation by the proteosome machinery, the cells recycling plant. With Rb out of the way, the cell now reproduces uncontrollably.
Karen Kreeger | EurekAlert!
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