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PubMed 19932096


Referenced in Channelpedia wiki pages of: none

Automatically associated channels: Kv10.1



Title: Calcitriol inhibits Ether-à go-go potassium channel expression and cell proliferation in human breast cancer cells.

Authors: Rocío García-Becerra, Lorenza Díaz, Javier Camacho, David Barrera, David Ordaz-Rosado, Angélica Morales, Cindy Sharon Ortiz, Euclides Avila, Enrique Bargallo, Myrna Arrecillas, Ali Halhali, Fernando Larrea

Journal, date & volume: Exp. Cell Res., 2010 Feb 1 , 316, 433-42

PubMed link: http://www.ncbi.nlm.nih.gov/pubmed/19932096


Abstract
Antiproliferative actions of calcitriol have been shown to occur in many cell types; however, little is known regarding the molecular basis of this process in breast carcinoma. Ether-à-go-go (Eag1) potassium channels promote oncogenesis and are implicated in breast cancer cell proliferation. Since calcitriol displays antineoplastic effects while Eag1 promotes tumorigenesis, and both factors antagonically regulate cell cycle progression, we investigated a possible regulatory effect of calcitriol upon Eag1 as a mean to uncover new molecular events involved in the antiproliferative activity of this hormone in human breast tumor-derived cells. RT real-time PCR and immunocytochemistry showed that calcitriol suppressed Eag1 expression by a vitamin D receptor (VDR)-dependent mechanism. This effect was accompanied by inhibition of cell proliferation, which was potentiated by astemizole, a nonspecific Eag1 inhibitor. Immunohistochemistry and Western blot demonstrated that Eag1 and VDR abundance was higher in invasive-ductal carcinoma than in fibroadenoma, and immunoreactivity of both proteins was located in ductal epithelial cells. Our results provide evidence of a novel mechanism involved in the antiproliferative effects of calcitriol and highlight VDR as a cancer therapeutic target for breast cancer treatment and prevention.