Regulation of the metastasis suppressor Nm23-H1 by tumor viruses

Naunyn Schmiedebergs Arch Pharmacol. 2015 Feb;388(2):207-24. doi: 10.1007/s00210-014-1043-8. Epub 2014 Sep 10.

Abstract

Metastasis is the most common cause of cancer mortality. To increase the survival of patients, it is necessary to develop more effective methods for treating as well as preventing metastatic diseases. Recent advancement of knowledge in cancer metastasis provides the basis for development of targeted molecular therapeutics aimed at the tumor cell or its interaction with the host microenvironment. Metastasis suppressor genes (MSGs) are promising targets for inhibition of the metastasis process. During the past decade, functional significance of these genes, their regulatory pathways, and related downstream effector molecules have become a major focus of cancer research. Nm23-H1, first in the family of Nm23 human homologues, is a well-characterized, anti-metastatic factor linked with a large number of human malignancies. Mounting evidence to date suggests an important role for Nm23-H1 in reducing virus-induced tumor cell motility and migration. A detailed understanding of the molecular association between oncogenic viral antigens with Nm23-H1 may reveal the underlying mechanisms for tumor virus-associated malignancies. In this review, we will focus on the recent advances to our understanding of the molecular basis of oncogenic virus-induced progression of tumor metastasis by deregulation of Nm23-H1.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Animals
  • Humans
  • NM23 Nucleoside Diphosphate Kinases / genetics
  • NM23 Nucleoside Diphosphate Kinases / metabolism*
  • Neoplasm Invasiveness
  • Neoplasm Metastasis*
  • Nerve Tissue Proteins / metabolism
  • Nuclear Proteins / metabolism
  • Oncogenic Viruses / physiology*

Substances

  • NM23 Nucleoside Diphosphate Kinases
  • Nerve Tissue Proteins
  • Nuclear Proteins
  • necdin