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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
Author(s) -
Hou Jianmei,
Wang Xudong,
Li Yang,
Liu Xiaohong,
Wang Zhuting,
An Jing,
Yang Li,
He Yan
Publication year - 2012
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2012.02.018
Subject(s) - mcf 7 , cyclin e , cyclin d , calpain , cyclin d1 , cyclin a , cyclin a2 , cyclin , cyclin b , cancer research , chemistry , cyclin b1 , breast cancer , microbiology and biotechnology , cell cycle , biology , cancer , medicine , cyclin dependent kinase 1 , human breast , biochemistry , enzyme
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.