It is suggested that GPER-associated signaling contributes to EMT-like phenotypic changes, migration, and invasion in GB.
Abstract
ABSTRACT Glioblastomas (GBs) are the most frequent and aggressive central nervous system tumors, whose progression is influenced by sex hormones. 17β-estradiol (E2), promotes an epithelial-to-mesenchymal transition (EMT)-like process and enhances proliferative, migratory, and invasive capacities in GB through intracellular estrogen receptors. However, the role of G protein–coupled estrogen receptor (GPER) in GB remains poorly understood. We evaluated the effects of E2, the GPER-agonist G-1, and the GPER-antagonist G-15 on EMT-related processes, migration, and invasion in U251 and U87 GB-derived cells. GPER activation by E2 and G-1 increased migration and invasion, whereas G-15, alone or combined, reduced these effects. GPER activation also induced a mesenchymal-like phenotype. These findings suggest that GPER-associated signaling contributes to EMT-like phenotypic changes, migration, and invasion in GB.
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