Recent studies reveal that estrogens act on cells and tissues, not only through two canonical estrogen receptors ERα and ERβ, but also through the receptor coupled with G proteins, named GPER, formerly GPR30, and member of seven transmembrane receptor superfamily. GPER was found to be implicated both in rapid non-genomic estrogen response and in transcriptional regulation. Effects of GPER include activation of MAPK and PI3K signaling pathways, stimulation of adenyl cyclase, and mobilization of calcium ions from intracellular stores, as well as upregulation of genes such as FOS and CTGF. Identification of agonists and antagonists of GPER allowed not only to shed light on the participation of estrogen signaling in the biology and pathobiology of hormone-dependent tissues, but also its importance in the estrogen and antiestrogen therapies. Antiestrogens tamoxifen, raloxifene, or fulvestrant proved,to be agonists of GPER, which undoubtedly is not without significance for the efficacy of the therapy.
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