Functional modulation of the metastatic suppressor Nm23-H1 by oncogenic viruses.

Abstract

Evidence over the last two decades from a number of disciplines has solidified some fundamental concepts in metastasis, a major contributor to cancer associated deaths. However, significant advances have been made in controlling this critical cellular process by focusing on targeted therapy. A key set of factors associated with this invasive phenotype is the nm23 family of over twenty metastasis-associated genes. Among the eight known isoforms, Nm23-H1 is the most studied potential anti-metastatic factor associated with human cancers. Importantly, a growing body of work has clearly suggested a critical role for Nm23-H1 in limiting tumor cell motility and progression induced by several tumor viruses, including Epstein-Barr virus (EBV), Kaposi's sarcoma associated herpes virus (KSHV) and human papilloma virus (HPV). A more in depth understanding of the interactions between tumor viruses encoded antigens and Nm23-H1 will facilitate the elucidation of underlying mechanism(s) which contribute to virus-associated cancers. Here, we review recent studies to explore the molecular links between human oncogenic viruses and progression of metastasis, in particular the deregulation of Nm23-H1 mediated suppression.

• Authors: Abhik Saha, Erle S Robertson
• Journal: FEBS letters (FEBS Lett) Vol. 585 Issue 20 Pg. 3174-84 (Oct 20 2011) ISSN: 1873-3468 [Electronic] England
• PMID: 21846466 (Publication Type: Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't, Review)
• Copyright: Copyright © 2011 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.

Chemical References

• Antigens, Neoplasm
• Antigens, Viral
• NM23 Nucleoside Diphosphate Kinases
• Tumor Suppressor Proteins
• NME1 protein, human

Topics

• Animals
• Antigens, Neoplasm (genetics, metabolism)
• Antigens, Viral (genetics, metabolism)
• Cell Movement
• Humans
• NM23 Nucleoside Diphosphate Kinases (genetics, metabolism)
• Neoplasm Metastasis
• Oncogenic Viruses (genetics, metabolism)
• Tumor Suppressor Proteins (genetics, metabolism)
• Tumor Virus Infections (enzymology, genetics, pathology)