Estrogen receptor expression and growth-promoting function in human choriocarcinoma cells

DNA Cell Biol. 1997 Aug;16(8):969-77. doi: 10.1089/dna.1997.16.969.

Abstract

Tamoxifen (1.0 microM) was found to inhibit the expression of a thymidine kinase (TK) promoter-reporter gene, lacking an estrogen response element (ERE), in transiently transfected BeWo cells, suggesting that inhibition of TK promoter activity was linked to secondary estrogen-dependent effects on BeWo cell function. Estradiol (0.05-0.45 microM) stimulated BeWo cell proliferation and increased the percentage of S-phase cells. Tamoxifen (1.35-4.05 microM) inhibited BeWo cell growth and antagonized the stimulatory actions of 0.15 microM estradiol. Reverse transcription-polymerase chain reaction and Western analyses confirmed the presence of estrogen receptor (ER) transcripts and the 67-kD ER in BeWo cells. The BeWo cell ER binds to an ERE consensus sequence and the ER-ERE complex is supershifted by antibodies directed against the ER. We conclude that BeWo cells express a functional ER that is important for the control of BeWo cell proliferation, suggesting a potential role for estrogens in mediating placental trophoblast growth and development.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Base Sequence
  • Binding Sites
  • COS Cells
  • Cell Cycle / drug effects
  • Cell Division / drug effects
  • Choriocarcinoma / metabolism*
  • Choriocarcinoma / pathology
  • DNA Primers
  • Estradiol / pharmacology*
  • Female
  • Gene Expression Regulation, Neoplastic
  • Genes, Reporter
  • Humans
  • Luciferases / biosynthesis
  • Oligodeoxyribonucleotides
  • Polymerase Chain Reaction
  • Pregnancy
  • Promoter Regions, Genetic
  • Receptors, Estrogen / biosynthesis
  • Receptors, Estrogen / physiology*
  • Recombinant Fusion Proteins / biosynthesis
  • Tamoxifen / pharmacology
  • Thymidine Kinase / biosynthesis
  • Thymidine Kinase / genetics
  • Transcription, Genetic
  • Transfection
  • Tumor Cells, Cultured
  • Uterine Neoplasms / metabolism*
  • Uterine Neoplasms / pathology

Substances

  • DNA Primers
  • Oligodeoxyribonucleotides
  • Receptors, Estrogen
  • Recombinant Fusion Proteins
  • Tamoxifen
  • Estradiol
  • Luciferases
  • Thymidine Kinase