[Study of Kinase Inhibitor WP1066 on the STAT3/JAK2 of Prostate Stromal Cells]

Sichuan Da Xue Xue Bao Yi Xue Ban. 2018 Jan;49(1):65-68.
[Article in Chinese]

Abstract

Objective: To study the role of JAK2 signaling pathway in prostate stromal cells and the effect of inhibitor WP1066 on its expression.

Methods: The phosphorylation of JAK2 and STAT3 in prostate tissues of patients with benign prostatic hyperplasia (BHP) (n=4) and severe histological prostatitis (HP) plus BPH (n=4) was tested by using Western blot to verify the activation of their mediated signaling pathway. Kinase inhibitor WP1066 was added to prostate stromal cells to detect inhibition of the JAK2 and STAT3 activation launched by IL-6.

Results: JAK2 phosphorylation level (pJAK2) was significantly increased in the patients with severe HP plus BPH,and the expression of JAK2 or STAT3 was not decreased in WP1066 treatment cells. However,neither phosphorylation in JAK2 nor STAT3 was able to be detected in the cells treated with WP1066 or WP1066+IL-6,indicating that the signaling pathway of JAK2-STAT3 was inhibited.

Conclusion: JAK/STAT signaling pathway is activated in patients with severe HP plus BPH , but could be inhibited by WP1066.

Keywords: Activation; Benign prostatic hyperplasia; Kinase inhibitor; Phosphorylation.

MeSH terms

  • Humans
  • Janus Kinase 2 / antagonists & inhibitors*
  • Male
  • Phosphorylation
  • Prostate / cytology*
  • Prostatic Hyperplasia / metabolism*
  • Pyridines / pharmacology*
  • STAT3 Transcription Factor / antagonists & inhibitors*
  • Signal Transduction
  • Stromal Cells / drug effects*
  • Tyrphostins / pharmacology*

Substances

  • Pyridines
  • STAT3 Transcription Factor
  • STAT3 protein, human
  • Tyrphostins
  • WP1066
  • JAK2 protein, human
  • Janus Kinase 2