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

Hou Jianmei | Zendy; Wang Xudong | Zendy; Li Yang | Zendy; Liu Xiaohong | Zendy; Wang Zhuting | Zendy; An Jing | Zendy; Yang Li | Zendy; He Yan | Zendy

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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 , calpain , breast cancer , cyclin e , cyclin d1 , cancer research , chemistry , microbiology and biotechnology , cancer , medicine , human breast , oncology , biology , biochemistry , cell cycle , 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.

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