論文

査読有り
2017年6月

Canine REIC/Dkk-3 interacts with SGTA and restores androgen receptor signalling in androgen-independent prostate cancer cell lines

BMC VETERINARY RESEARCH
  • Yuiko Kato
  • ,
  • Kazuhiko Ochiai
  • ,
  • Shota Kawakami
  • ,
  • Nobuhiro Nakao
  • ,
  • Daigo Azakami
  • ,
  • Makoto Bonkobara
  • ,
  • Masaki Michishita
  • ,
  • Masami Morimatsu
  • ,
  • Masami Watanabe
  • ,
  • Toshinori Omi

13
1
開始ページ
170
終了ページ
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1186/s12917-017-1094-4
出版者・発行元
BIOMED CENTRAL LTD

Background: The pathological condition of canine prostate cancer resembles that of human androgen-independent prostate cancer. Both canine and human androgen receptor (AR) signalling are inhibited by overexpression of the dimerized co-chaperone small glutamine-rich tetratricopeptide repeat-containing protein a (SGTA), which is considered to cause the development of androgen-independency. Reduced expression in immortalised cells (REIC/Dkk-3) interferes with SGTA dimerization and rescues AR signalling. This study aimed to assess the effects of REIC/Dkk-3 and SGTA interactions on AR signalling in the canine androgen-independent prostate cancer cell line CHP-1.
Results: Mammalian two-hybrid and Halo-tagged pull-down assays showed that canine REIC/Dkk-3 interacted with SGTA and interfered with SGTA dimerization. Additionally, reporter assays revealed that canine REIC/Dkk-3 restored AR signalling in both human and canine androgen-independent prostate cancer cells. Therefore, we confirmed the interaction between canine SGTA and REIC/Dkk-3, as well as their role in AR signalling.
Conclusions: Our results suggest that this interaction might contribute to the development of a novel strategy for androgen-independent prostate cancer treatment. Moreover, we established the canine androgen-independent prostate cancer model as a suitable animal model for the study of this type of treatment-refractory human cancer.

Web of Science ® 被引用回数 : 3

リンク情報
DOI
https://doi.org/10.1186/s12917-017-1094-4
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/28599655
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000402978200003&DestApp=WOS_CPL

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