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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
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.
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页码:892 / 896
页数:5
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