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

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.

► We addressed whether and how 17β-estradiol (E2) modulates cyclin E in MCF-7 cells.
► E2-induced both up-regulation and processing of cyclin E.
► Estrogenic alcohol also triggered cyclin E truncation.
► E2-induced effects could be significantly suppressed by calpain inhibitors.