Análisis de la participación del receptor de estrógenos ERa/ErB y GPR30 en la translocación nuclear de Rac1 en la línea celular HaCaT.

Abstract

The GTPase Rac1 is a member of the Rho family, which plays a fundamental role in various cellular processes such as cell migration and invasion, cell adhesion, polymerization of actin filaments. In cancer, Rac1 participates in epithelial-mesenchymal transition, angiogenesis and promoting the invasive capacity of cells. Rac1 functions at the cytoplasmic level have been widely studied, but its participation in other cellular compartments has been poorly investigated. Several studies demonstrated that Rac1 can be translocated to the nucleus; however, little is known about the mechanism of Rac1 nuclear-cytoplasm shuttling and its function in the nucleus. Rac1 nuclear import is dependent on its interaction whit proteins such as the importin karyopherin ¿2 and can be induced in response to stimuli such as epidermal growth factor. On the other hand, it is known that estrogens induce the nuclear translocation of Rac1; however, it is unknown which of the three estrogen receptors is necessary for this process. Objective: To evaluate the participation of the estrogen receptors ERa and ERB in the translocation of Rac1 to the nucleus in HaCaT cells. Methodology: HaCaT cells were transfected with a GFP-Rac1 expression plasmid and stimulated with estrogens in the presence or not of a chemical inhibitor for ERa and ERB. The subcellular localization of Rac1 was determined by fluorescence microscopy and cellular fractionation. Results: Our results indicate that the nuclear translocation of Rac1 in response to estrogens in HaCat cells, is not dependent on ERa or ERB, and suggest that it may be depend on GPR30 receptor. Conclusions: Rac1 translocates to the nucleus in estrogen-stimulated HaCaT cells. The estrogen receptors ERa or ERB, do not participate in the translocation of Rac1 to the nucleus in response to estrogens.