Premium
The role of GPR30 in breast cancer cell migration
Author(s) -
Doran Heather,
Ross Ruth A
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.1038.9
Subject(s) - gper , skbr3 , estrogen receptor , cancer research , breast cancer , cell migration , actin cytoskeleton , receptor , g protein coupled receptor , microbiology and biotechnology , chemistry , biology , cell , cancer , signal transduction , medicine , cytoskeleton , biochemistry , human breast
Some cells, although lacking the canonical estrogen receptors (ERs) still display rapid non‐genomic signalling in response to estrogen. Recently, a G protein coupled receptor; GPR30 (or GPER) and an alternative splice variant of the traditional ERα (ERα36) have been proposed as alternative estrogen receptors that may mediate these non‐genomic effects. This study investigated the role of GPR30 and ERα36 in breast cancer cell migration. Using a combination of cell migration assays, actin polymerisation measurements and immuno‐fluorescence we have demonstrated that SKBr3 cells (a ER receptor negative, breast cancer cell line) migrate towards the GPR30/ERα36 agonist G‐1; an effect that is attenuated by G‐15, a GPR30/ERα36 antagonist and pERK inhibitors, but not by ROCK inhibitors. We have also demonstrated that G‐1 activates a rapid signalling pathway involving changes in the actin cytoskeleton. The findings may progress the development of new therapeutics targeting ER negative breast cancer tumors. This research was sponsored by Selcia Limited (Ongar, Essex) and the University of Aberdeen