17beta-estradiol induces both up-regulation and processing of cyclin E in a calpain-dependent manner in MCF-7 breast cancer cells

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• 作者：Jianmei Hou^a ; Xudong Wang^a ; ^{xdwang@gmc.edu.cn} ; Yang Li^a ; Xiaohong Liu^a ; Zhuting Wang^b ; Jing An^a ; Li Yang^a ; Yan He^c
• 关键词：17beta-estradiol ; Cyclin E ; Calpain ; Proteolysis ; Up-regulation ; Breast cancer cell
• 刊名：FEBS Letters
• 出版年：2012
• 期刊代码：70_00145793
• 类别：bio
• 出版时间：23 March, 2012
• 卷：586
• 期：6
• 页码：892-896
• 文件大小：631 K

摘要

In the current study, we investigated whether 17beta-estradiol (E2) induces cyclin E expression and triggers cyclin E processing via calpain in MCF-7 breast cancer cells. We found that E2 induced increased expression of cyclin E in a slow and persistent manner, and a rapid yet sustained processing of cyclin E. In addition, estrogenic ethanol was able to stimulate cyclin E truncation. Calpeptin or ALLN greatly suppressed the E2-triggered cyclin E processing and its expression, suggesting a calpain-mediated action for E2. Finally, the E2-induced effects could also be significantly suppressed by BAPTA or U0126, indicating involvement of calcium/ERK signaling. Taken together, these results show that estrogen may contribute to both up-regulation and proteolysis of cyclin E through calpain in MCF-7 cells.