17beta-estradiol induces both up-regulation and processing of cyclin E in a calpain-dependent manner in MCF-7 breast cancer cells
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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DOI：
10.1016/j.febslet.2012.02.018
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发表时间：
2012-03-23
期刊：
影响因子：
3.5
通讯作者：
He, Yan
中科院分区：
文献类型：
--
作者：
Hou, Jianmei;Wang, Xudong;He, Yan
在目前的研究中，我们调查了17 β-雌二醇（E2）是否诱导细胞周期蛋白E的表达，并触发细胞周期蛋白E处理通过钙蛋白酶在MCF-7乳腺癌细胞。我们发现E2以缓慢和持续的方式诱导细胞周期蛋白E的表达增加，以及细胞周期蛋白E的快速而持续的加工。此外，雌激素乙醇能够刺激细胞周期蛋白E截短。Calpeptin或ALLN极大地抑制了E2触发的细胞周期蛋白E的加工及其表达，表明钙蛋白酶介导的E2作用。最后，BAPTA或U 0126也可显著抑制E2诱导的效应，表明钙/ERK信号通路参与。总之，这些结果表明，雌激素可能有助于MCF-7细胞中细胞周期蛋白E的上调和蛋白水解通过钙蛋白酶。(C)2012年欧洲生物化学学会联合会。Elsevier B. V.出版，保留所有权利。
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. (C) 2012 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.