Fig. 6.

PKC is the upstream mediator of GnRH-induced MAPK signaling and EGFR transactivation in EVTs. A and B, The EVTs that were serum-starved as described were stimulated with GnRH I or GnRH II (100 nm, 10 min) in the presence or absence of 30-min pretreatment with vehicle (0.1% DMSO) or GF109203X (5 μm, a PKC inhibitor). The phosphorylation of ERK1/2 (A) or JNK (B) was detected by Western blotting with specific antibodies. C, Invasive capacity of EVTs that were treated with GnRH I or GnRH II (100 nm) in the presence or absence of pretreatment with vehicle (0.1% DMSO) or GF109203X (5 μm) were analyzed by invasion assay. D, The EVTs that were serum starved as described were stimulated with GnRH II (100 nm, 10min) in the presence or absence of pretreatment with vehicle (0.1% DMSO), AG1478 (5 μm), or GF109203X (5 μm). The phosphorylation of EGFR was determined by Western blotting with specific antibody. The data derived from at least three separate sets of experiments were standardized to the corresponding control, and the statistical results are presented in the column graphs. a, P < 0.05 vs. control; b, P < 0.05 vs. treatment with GnRH I alone; c, P < 0.05 vs. treatment with GnRH II alone.