Universidad de Guadalajara Guadalajara, Jalisco, Mexico
Abstract Text: Prostate cancer (PCa) is clinical problem worldwide and its molecular mechanisms are still studied. Metastasis is common in these patients. Recently, G-protein coupled estrogen receptor (GPER) act as a growth modulator but it’s reported to control metastasis, by inducing signaling pathways activation, mainly mitogen-activated protein kinase (MAPK), phosphoinositide 3-kinase (PI3K) involved in migration and invasion. Agonist molecules like G1 was identified to induced a conformational change in GPER which prevents its activity depending on the type of tissue, therefore GPER on cellular processes is extremely heterogeneous and needs to be studied for each type of cancer, however, in PCa is not well elucidated. Evaluate ERK and AKT signaling expression and their relationship between migration and invasion in LNCaP prostate cell lines. LNCaP cell line were grown and stimulated with G1 and E2, to subsequently performed protein extraction and evaluate ERK and AKT phosphorylated expression using Western Blot technique. Also, with the same stimuli, migration and invasion assays were performed by transwell plates. The expression of phosphorylated molecules were observed. For LNCaP AKT3 isoform remains constant in all treatments while in pERK (ERK1) decreases with G1 treatment compare to control. LNCaP migration was observed to decrease 33% with G1 and 50% with E2 compare to control with a significant p< 0.001, meanwhile invasion prevailed for both treatments being 60% with G1 with a significant p< 0.01 and 93% with E2 compare to control. In this research, G1 treatment affect ERK1 activity which decrease migration and invasion in LNCaP cells.
