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

Michelle Kirby, A. Zsarnovszky, Scott M. Belcher

Research output: Contribution to journalArticle

16 Citations (Scopus)

Abstract

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 ERα and ERβ are expressed in PFSK1 cells. The ability of estrogen to rapidly activate MAPK signaling was tested; low physiological concentrations of E2 stimulated ERK1/2 phosphorylation and nuclear translocation within 15min of exposure. Exogenously added 17β-estradiol (E2) could not stimulate PFSK1 growth, however E2 significantly increased PFSK1 cell migration, suggesting that rapid actions of E2 and ER-mediated processes might contribute to the metastatic phenotype of some PNETs.

Original languageEnglish
Pages (from-to)753-758
Number of pages6
JournalBiochemical and Biophysical Research Communications
Volume319
Issue number3
DOIs
Publication statusPublished - Jul 2 2004

Fingerprint

Primitive Neuroectodermal Tumors
Tumor Cell Line
Estrogen Receptors
Cerebral Cortex
Cell Movement
Tumors
Estrogens
Chemical activation
Cells
Brain Neoplasms
Cerebellum
Brain
Neuroepithelial Cells
Phosphorylation
Pediatrics
Cerebrum
Immune Sera
Estradiol
Phenotype
Cell Line

Keywords

  • ERα
  • ERβ
  • ERK1/2
  • Estrogen
  • Estrogen receptor
  • Growth
  • Hormone responsive
  • MAPK
  • Migration
  • Non-genomic
  • PNET
  • Signal transduction

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Molecular Biology

Cite this

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abstract = "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 ERα and ERβ are expressed in PFSK1 cells. The ability of estrogen to rapidly activate MAPK signaling was tested; low physiological concentrations of E2 stimulated ERK1/2 phosphorylation and nuclear translocation within 15min of exposure. Exogenously added 17β-estradiol (E2) could not stimulate PFSK1 growth, however E2 significantly increased PFSK1 cell migration, suggesting that rapid actions of E2 and ER-mediated processes might contribute to the metastatic phenotype of some PNETs.",
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AB - 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 ERα and ERβ are expressed in PFSK1 cells. The ability of estrogen to rapidly activate MAPK signaling was tested; low physiological concentrations of E2 stimulated ERK1/2 phosphorylation and nuclear translocation within 15min of exposure. Exogenously added 17β-estradiol (E2) could not stimulate PFSK1 growth, however E2 significantly increased PFSK1 cell migration, suggesting that rapid actions of E2 and ER-mediated processes might contribute to the metastatic phenotype of some PNETs.

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