Figure 2
Effects of GnRH-II antagonist treatment on apoptotic signaling in GnRH-I receptor-positive (wild-type; WT) and GnRH-I receptor-negative (GnRH-I receptor knockdown; KD) human breast cancer cells in vitro. (a) Amount of phosphorylated p38 after treatment without or with GnRH-II antagonist [Ac-D2Nal1, D-4Cpa2, D-3Pal3,6, Leu8, D-Ala10]GnRH-II (10-7 M) in nontransfected MCF-7 breast cancer cells and in MCF-7 breast cancer cells after knockdown of GnRH-I receptor expression. These are representative data obtained from three independent experiments in three different passages of the cell line. Experiments using MDA-MB-231 human breast cancer cells gave identical results. (b) Percentage of caspase-3 activity after 48 h of treatment of GnRH-I receptor-positive (wild-type; WT) and GnRH-I receptor-negative (GnRH-I receptor knockdown; KD) MDA-MB-231 breast cancer cells without (control = 100%) or with cytotoxic agent doxorubicin (10-9 M; positive control) or with GnRH-II antagonist [Ac-D2Nal1, D-4Cpa2, D-3Pal3, D-Lys6, D-Ala10]GnRH-II (10-7 M and 10-9 M). Columns represent mean ± SEM of data obtained from three independent experiments in three different passages of the cell line. (a) P < 0.001 versus control; (b) P < 0.01 versus control; (c) P < 0.05 versus control.