Premium
Decitabine inhibits tumor cell proliferation and up‐regulates e‐cadherin expression in Epstein–Barr virus‐associated gastric cancer
Author(s) -
Nakamura Munetaka,
Nishikawa Jun,
Saito Mari,
Sakai Kouhei,
Sasaki Sho,
Hashimoto Shinichi,
Okamoto Takeshi,
Suehiro Yutaka,
Yamasaki Takahiro,
Sakaida Isao
Publication year - 2017
Publication title -
journal of medical virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.782
H-Index - 121
eISSN - 1096-9071
pISSN - 0146-6615
DOI - 10.1002/jmv.24634
Subject(s) - decitabine , demethylating agent , apoptosis , cancer research , cell growth , lytic cycle , biology , azacitidine , dna methylation , virus , virology , gene expression , gene , genetics
The present study investigated the effect of a DNA demethylating agent, decitabine, against Epstein–Barr virus‐associated gastric cancer (EBVaGC). Decitabine inhibited cell growth and induced G2/M arrest and apoptosis in EBVaGC cell lines. The expression of E‐cadherin was up‐regulated and cell motility was significantly inhibited in the cells treated with decitabine. The promoter regions of p73 and RUNX3 were demethylated, and their expression was up‐regulated by decitabine. They enhanced the transcription of p21, which induced G2/M arrest and apoptosis through down‐regulation of c‐Myc. Decitabine also induced the expression of BZLF1 in SNU719. Induction of EBV lytic infection was an alternative way to cause apoptosis of the host cells. This study is the first report to reveal the effectiveness of a demethylating agent in inhibiting tumor cell proliferation and up‐regulation of E‐cadherin in EBVaGC. J. Med. Virol. 89:508–517, 2017 . © 2016 Wiley Periodicals, Inc.