Send to

Choose Destination
Cancer Lett. 2005 Mar 18;220(1):57-65.

Estradiol-induced ezrin overexpression in ovarian cancer: a new signaling domain for estrogen.

Author information

Department of Obstetrics and Gynecology, Yale University, P.O. Box 208063, 333 Cedar Street, FMB 331, New Haven, CT 06520-8063, USA.


We have for the first time exposed estrogen's role in the epithelial ovarian cancer (OVCA) metastatic cascade and discovered that it is related to the induction of ezrin over-expression. 17beta Estradiol (E2) was administered to SKOV3 (ERalpha>beta) and DOV13 (ERalpha<ERbeta) OVCA cells in serum-and phenol red-free medium fortified with transferrin and insulin. Incubated cells that penetrated Matrigel membranes were counted, immunostained and analyzed for immunoreactive ezrin. E2 induced an invasive phenotype with translocation of ezrin to cell edges, including pseudopodia and ruffles. A strong correlation was found between ezrin expression and Matrigel penetration induced by E2. Increases in cell number and ezrin expression were confirmed by flask incubations. E2 stimulation of OVCA cell proliferation, motility and Matrigel penetration was dose-related and raloxifene or tamoxifen blocked E2's effect, supporting an ER action. This previously unreported effect of estrogen on ezrin expression may play a role in the clinical course of estrogen-sensitive cancers and other normal or diseased cell actions.

[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center