激酶抑制剂WP1066对前列腺基质细胞STAT3/JAK2的研究

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

作者信息

Li Yun-Xiang, Li Jin-Ming, Wei Qiang, Zhang Zong-Ping, Wu Ji, Wang An-Guo

机构信息

Department of Urology,Nanchong Central Hospital,Nanchong 637000,China.

Department of Urology,West China Hospital,Sichuan University,Chengdu 610041,China.

出版信息

Sichuan Da Xue Xue Bao Yi Xue Ban. 2018 Jan;49(1):65-68.

PMID:29737092

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) (=4) and severe histological prostatitis (HP) plus BPH (=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.

摘要

目的

研究JAK2信号通路在前列腺基质细胞中的作用以及抑制剂WP1066对其表达的影响。

方法

采用蛋白质免疫印迹法检测良性前列腺增生（BHP）患者（n = 4）及重度组织学前列腺炎（HP）合并BPH患者（n = 4）前列腺组织中JAK2和STAT3的磷酸化水平，以验证其介导的信号通路的激活情况。向前列腺基质细胞中加入激酶抑制剂WP1066，检测其对IL - 6引发的JAK2和STAT3激活的抑制作用。