SPRY4-mediated ERK1/2 signaling inhibition abolishes 17β-estradiol-induced cell growth in endometrial adenocarcinoma cell.

Objective: Basic fibroblast growth factor (FGF2)-mediated Extracellular signal-regulated kinases1/2 (ERK1/2) signaling is a critical modulator in angiogenesis. SPRY4 has been reported to be a feedback negative regulator of FGFs-induced ERK1/2 signaling. The aim of this study was to explore the role of SPRY4 in endometrial adenocarcinoma cell. Materials and methods: The effect of SPRY4 expression on FGF2-mediated ERK1/2 signaling was detected by luciferase assay and Western blot analysis. The growth of Ishikawa cells was detected using colony formation assay and cell number counting experiment. Results: We found that plasmid-driven SPRY4 expression efficiently blocked the activity of FGF2-induced ERK1/2 signaling in Ishikawa cells. SPRY4 expression significantly reduced the proliferation and 17β-estradiol-induced proliferation of Ishikawa cells. Conclusion: SPRY4 may function as a tumor suppressor in endometrial adenocarcinoma. 目的：碱性成纤维细胞生长因子(FGF2)介导的细胞外信号调节激酶(ERK1/2)信号转导是血管发生过程中的关键调节器。有报道显示SPRY4是FGFs介导的ERK1/2信号转导的负反馈调节蛋白。本研究的目的是探讨SPRY4在子宫内膜腺癌细胞发生中的作用。 材料与方法：采用荧光素酶检测与蛋白印迹分析方法探测SPRY4在FGF2介导的ERK1/2信号转导过程中的表达效果。采用克隆形成实验与细胞计数实验检测Ishikawa细胞的生长情况。 结果：我们发现在Ishikawa细胞，质粒驱动的SPRY4表达有效地阻滞了FGF2介导的ERK1/2信号转导。SPRY4的表达显著降低了Ishikawa细胞增殖和17-β-雌二醇诱导的Ishikawa细胞增殖。 结论：SPRY4可能具有子宫内膜腺癌抑癌基因的功能。 [ABSTRACT FROM AUTHOR]