Abstract | OBJECTIVE: METHODS: MCF-7 breast cancer cells were treated with ERKl/2 inhibitor ( PD98059) or CANP inhibitor ( calpeptin) before exposure to 1×10(-8) M E2. MTT colorimetry and flow cytometry were used to analyze effects on cell proliferation and cell cycle progression, respectively. Expression of phosphorylated-ERK (p-ERK), total ERK, and Capn4 proteins were assessed by Western blotting. RESULTS: Cell proliferation increased in cells treated with E2 for 24 h (P<0.05), and the proportion of cells in G0/G1 was decreased, accompanied by accelerated G1/S. Calpeptin pre-treatment significantly inhibited the E2-induced proliferation of MCF-7 cells (P<0.05), while also ameliorating the effects of E2 on cell cycle progression. Further, expression of p-ERK was rapidly up-regulated (after 10 min) by E2 (P<0.05), an effect that persisted 16 h after E2 exposure but which was significantly inhibited by PD98059 (P<0.05). CONCLUSIONS: Finally, expression of Capn4 protein was rapidly up-regulated in E2-exposed cells (P<0.05), but this change was significantly inhibited by PD98059 or calpeptin (P<0.05) pre-treatment. Thus, the rapid, non-genomic ERK/CANP signaling pathway mediates E2-induced proliferation of human breast cancer cells.
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Authors | Guo-Sheng Wang, Yan-Gang Huang, Huan Li, Shi-Jie Bi, Jin-Long Zhao |
Journal | International journal of clinical and experimental medicine
(Int J Clin Exp Med)
Vol. 7
Issue 1
Pg. 156-62
( 2014)
ISSN: 1940-5901 [Print] United States |
PMID | 24482702
(Publication Type: Journal Article)
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