論文

査読有り
2016年8月

ALKBH8 promotes bladder cancer growth and progression through regulating the expression of survivin

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
  • Ikumi Ohshio
  • Ryoji Kawakami
  • Yohei Tsukada
  • Kazuhiro Nakajima
  • Kaori Kitae
  • Tomoki Shimanoe
  • Yasuka Saigo
  • Hiroaki Hase
  • Yuko Ueda
  • Kentaro Jingushi
  • Kazutake Tsujikawa
  • 全て表示

477
3
開始ページ
413
終了ページ
418
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1016/j.bbrc.2016.06.084
出版者・発行元
ACADEMIC PRESS INC ELSEVIER SCIENCE

Human AlkB homolog 8 (ALKBH8) is highly expressed in high-grade, superficially and deeply invasive bladder cancer. Moreover, ALKBH8 knockdown induces apoptosis in bladder cancer cells. However, the underlying anti-apoptotic mechanism of ALKBH8 in bladder cancer cells has thus far remained unclear. Moreover, there is no direct evidence that highly expressed ALKBH8 is involved in tumor progression in vivo. We here show that ALKBH8 knockdown induced apoptosis via downregulating the protein expression of survivin, an anti-apoptotic factor also exhibiting increased levels in bladder cancer. We also clarify that ALKBH8 transgenic mice showed an accelerated rate of bladder tumor mass and invasiveness in an N-butyl-N-(4-hydroxybutyl)-nitrosamine-induced bladder cancer model. These findings suggest that the high expression of ALKBH8 is critical for the growth and progression of bladder cancer. (C) 2016 Elsevier Inc. All rights reserved.

リンク情報
DOI
https://doi.org/10.1016/j.bbrc.2016.06.084
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/27329810
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000380732000017&DestApp=WOS_CPL
ID情報
  • DOI : 10.1016/j.bbrc.2016.06.084
  • ISSN : 0006-291X
  • eISSN : 1090-2104
  • PubMed ID : 27329810
  • Web of Science ID : WOS:000380732000017

エクスポート
BibTeX RIS