Objective      To explore the effects of activated estrogen/GPR30/ERK signaling on the migration and invasion of triple-negative breast cancer (TNBC) cell line MDA-MB-468.        Methods      Immunofluorescent assay and Western blotting were used to test the expression and localization of estrogen receptor GPR30 in MDA-MB-468 cells. The expression level of phospho-extracellular regulate kinase (p-ERK) was detected by Western blotting. The changes of cell migration and invasion ability were examined by wound-healing assay and Transwell assay

respectively.       Results      Estrogen receptor GPR30 was detected with high expression level in MDA-MB-468 cells and was mostly expressed in the cytoplasm. After treating with 17-β estradiol (E2) and GPR30 specific agonist (G1)

the GPR30/ERK signaling was remarkably activated. The relative protein expressions of p-ERK in the E2 and G1 treatment groups were (2.07±0.11) and (1.98±0.06) times higher than those of the control group (P0.05)

respectively. Moreover

E2 and G1 significantly increased the ability of cell migration. The relative migrated cell numbers in the E2 and G1 treatment groups were 2.10±0.20 and 2.14±0.34 times higher than those of the control group (P0.05)

respectively. Transwell assays indicated the similar results as wound-healing assays. Interestingly

these changes induced by E2 and G1 could be significantly blocked by GPR30 specific antagonist (G15) and ERK specific inhibitor (U0126) (P0.05).       Conclusion      Estrogen increases the ability of cell migration and invasion through activating GPR30/ERK signaling in TNBC cells. Inhibition of estrogen/GPR30/ERK signaling represents a novel targeted therapy in TNBC.