Epstein-Barr Virus Genome Replication as a Molecular Target for Cancer Therapy

Kohji Noguchi

Research output: Contribution to journalArticle

Abstract

Epstein-Barr virus (EBV), a human oncogenic virus, is a B cell-tropic herpesvirus and has the ability to immortalize normal B cells during latent infection. The Epstein-Barr nuclear antigen 1 (EBNA1) protein of EBV is expressed in the most EBV latently infected cells and binds to a specific viral genome region termed "oriP" (origin of plasmid replication) to maintain the stability of the approximately 170 kb double-stranded circular virus genomic DNA (episome) in cells. EBV elimination is thought to inhibit progression of EBV-associated malignancies, and the EBNA1-dependent mechanisms for EBV episome replication and maintenance are considered to be novel molecular targets for anti-EBV therapy. We have explored small-molecule compounds that can inhibit the binding between EBNA1 protein and oriP and found one pyrrole imidazole polyamide named DSE3 which can also inhibit EBV-mediated immortalization of normal B cells. These data suggested that an EBNA1-targeting strategy could be useful to combat EBV-associated malignancies.

Original languageEnglish
Pages (from-to)63-67
Number of pages5
JournalYakugaku zasshi : Journal of the Pharmaceutical Society of Japan
Volume139
Issue number1
DOIs
Publication statusPublished - 2019 Jan 1

Fingerprint

Virus Replication
Human Herpesvirus 4
Genome
Nuclear Antigens
Neoplasms
Plasmids
B-Lymphocytes
Therapeutics
Oncogenic Viruses
Pyrroles
Replication Origin
DNA Viruses
Viral Genome
Herpesviridae
Nylons
Proteins
Maintenance
Infection

Keywords

  • DNA replication
  • Epstein-Barr virus
  • molecular target

ASJC Scopus subject areas

  • Pharmacology
  • Pharmaceutical Science

Cite this

Epstein-Barr Virus Genome Replication as a Molecular Target for Cancer Therapy. / Noguchi, Kohji.

In: Yakugaku zasshi : Journal of the Pharmaceutical Society of Japan, Vol. 139, No. 1, 01.01.2019, p. 63-67.

Research output: Contribution to journalArticle

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