Role of the G protein/ROCK/moesin pathway for ER+ breast cancer cell invasion.

<p>Steroid-deprived, growth synchronized ER+ T47-D cells were exposed to 10 nM E2, or 10 nM E2-BSA conjugate in the presence or absence of the ER antagonist ICI 182,720 (ICI; 1 µM), of the G protein inhibitor PTX (100 ng/ml), or of the ROCK-2 inhibitor, Y-27632 (Y; 10 µM) or of the selective estrogen receptor modulator (SERM) tamoxifen (TAM, 10 nM). In addition, some T47-D cells were treated with 10 nM E2 in the presence or absence of transfection with sense (Sense; 2 µM) or antisense (AS; 2 µM) moesin phosphorotioate oligonucleotides (PONs). Breast cancer cell invasion through matrigel was assayed by using invasion chambers. Invading cells were counted in the central field of triplicate membranes. Invasion indexes and representative images in chambers with matrigel are shown. * = p<0.05 vs. E2.