Oncogenic Epstein-Barr virus recruits Nm23-H1 to regulate chromatin modifiers

Lab Invest. 2018 Feb;98(2):258-268. doi: 10.1038/labinvest.2017.112. Epub 2017 Oct 16.

Abstract

In cancer progression, metastasis is a major cause of poor survival of patients and can be targeted for therapeutic interventions. The first discovered metastatic-suppressor Nm23-H1 possesses nucleoside diphosphate kinase, histidine kinase, and DNase activity as a broad-spectrum enzyme. Recent advances in cancer metastasis have opened new ways for the development of therapeutic molecular approaches. In this review, we provide a summary of the current understanding of Nm23/NDPKs in the context of viral oncogenesis. We also focused on Nm23-H1-mediated cellular events with an emphasis on chromatin modifications. How Nm23-H1 modulates the activities of chromatin modifiers through interaction with Epstein-Barr virus-encoded oncogenic antigens and related crosstalks are discussed in the context of other oncogenic viruses. We also described the current understanding of the cellular and viral interactions of Nm23-H1 and their reference to transcription regulation and metastasis. Further, we summarized the recent therapeutic approaches targeting Nm23 and its potential links to pathways that can be exploited by oncogenic viruses.

Publication types

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

MeSH terms

  • Carcinogenesis / genetics*
  • Chromatin / genetics*
  • Chromatin / metabolism
  • Gene Expression Regulation, Neoplastic*
  • Herpesvirus 4, Human / genetics*
  • Herpesvirus 4, Human / metabolism
  • Humans
  • Models, Genetic
  • NM23 Nucleoside Diphosphate Kinases / genetics*
  • NM23 Nucleoside Diphosphate Kinases / metabolism
  • Neoplasm Metastasis
  • Neoplasms / genetics
  • Neoplasms / metabolism
  • Neoplasms / pathology
  • Protein Binding

Substances

  • Chromatin
  • NM23 Nucleoside Diphosphate Kinases