中国神经再生研究(英文版) ›› 2012, Vol. 7 ›› Issue (4): 283-289.

• 原著:神经损伤修复保护与再生 • 上一篇    下一篇

Effects of fulvestrant on biological activity and Wnt expression in rat GH3 cells

  

  • 收稿日期:2011-09-24 修回日期:2011-11-22 出版日期:2012-02-05 发布日期:2012-02-05

Effects of fulvestrant on biological activity and Wnt expression in rat GH3 cells

Jiwei Bai1, Yan Wang2, Chuzhong Li1, Yazhuo Zhang1   

  1. 1 Beijing Neurosurgical Institute, Capital Medical University, Beijing 100050, China
    2 Center of Clinical Genetics, Affiliated Bayi Children’s Hospital, General Hospital of Beijing Military Command of Chinese PLA, Beijing 100700, China
  • Received:2011-09-24 Revised:2011-11-22 Online:2012-02-05 Published:2012-02-05
  • Contact: Yazhuo Zhang, M.D., Chief physician, Professor, Beijing Neurosurgical Institute, Capital Medical University, Beijing 100050, China zyz2004520@126.com
  • About author:Jiwei Bai☆, M.D., Beijing Neurosurgical Institute, Capital Medical University, Beijing 100050, China

Abstract:

The present study investigated the influence of anti-estrogen treatment (fulvestrant) on pituitary adenoma cell line GH3 biological activity, the estrogen receptor α pathway, the WnT pathway, and mechanisms of decreased Wnt inhibitory factor-1 expression in GH3 cells. Results showed that fulvestrant suppressed GH3 cell proliferation and reduced hormone secretion in a dose-dependent manner. Estrogen receptor α and Wnt4 expression decreased, but Wnt inhibitory factor-1 expression increased in a dose-dependent manner following fulvestrant treatment, and β-catenin expression remained unchanged. Inhibitors of DNA methylation and histone modification upregulated Wnt inhibitory factor-1 expression. Results suggested that fulvestrant suppressed biological activity of GH3 cells via the estrogen receptor α and Wnt pathways. These results suggested that decreased Wnt inhibitory factor-1 expression in GH3 cells played a role in epigenetic mechanisms. Anti-estrogen therapies could provide novel treatments for growth hormone adenomas.

Key words: β-catenin, estrogen, estrogen receptor α, GH3 cell line, Wnt inhibitory factor-1, Wnt4