Estrogen receptor expression in a human primitive neuroectodermal tumor cell line from the cerebral cortex: estrogen stimulates rapid ERK1/2 activation and receptor-dependent cell migration.

Primitive neuroectodermal tumors (PNETs) are the most common form of pediatric brain tumor. Most often these malignant childhood brain tumors arise from neuroepithelial precursor cells in the cerebellum, and less frequently in the cerebral cortex. Because the normal PNET precursor cells from the cerebrum and cerebellum transiently express high levels of estrogen receptors (ERs), we hypothesized that the PNET cells of the cerebrocortical-derived cell line PFSK1 may also express ERs and would be responsive to estrogen. Results of immunoblot studies using ER-specific antiserum indicate that both ERalpha and ERbeta are expressed in PFSK1 cells. The ability of estrogen to rapidly activate MAPK signaling was tested; low physiological concentrations of E(2) stimulated ERK1/2 phosphorylation and nuclear translocation within 15min of exposure. Exogenously added 17beta-estradiol (E(2)) could not stimulate PFSK1 growth, however E(2) significantly increased PFSK1 cell migration, suggesting that rapid actions of E(2) and ER-mediated processes might contribute to the metastatic phenotype of some PNETs.