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

被引：18
|
作者：
Hou, Jianmei [1 ]
Wang, Xudong [1 ]
Li, Yang [1 ]
Liu, Xiaohong [1 ]
Wang, Zhuting [2 ]
An, Jing [1 ]
Yang, Li [1 ]
He, Yan [3 ]
机构：
[1] Guiyang Med Univ, Sch Basic Med, Canc Res Grp, Dept Physiol, Guiyang 550004, Guizhou, Peoples R China
[2] Guiyang Med Univ, Sch Basic Med, Dept Biochem, Guiyang 550004, Guizhou, Peoples R China
[3] Guiyang Med Univ, Prov Key Lab Mol Biochem, Guiyang 550004, Guizhou, Peoples R China
来源：
FEBS LETTERS | 2012年 / 586卷 / 06期
基金：
中国国家自然科学基金;
关键词：
17beta-estradiol; Cyclin E; Calpain; Proteolysis; Up-regulation; Breast cancer cell; MOLECULAR-WEIGHT FORMS; SIGNALING PATHWAY; ACTIVATION; SURVIVAL; ESTROGEN; TUMOR; EXPRESSION; CARCINOMA; ISOFORMS; CALCIUM;
D O I：
10.1016/j.febslet.2012.02.018
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
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. (C) 2012 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
引用
收藏
页码：892 / 896
页数：5
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