Alterations in phosphoinositide metabolism associated with 17 β-estradiol and growth factor treatment of MCF-7 breast cancer cells

Carl E. Freter, Marc E. Lippman, Andrea Cheville, Sydelle Zinn, Edward P. Gelmann

Research output: Contribution to journalArticle

52 Scopus citations

Abstract

Steady-state levels of phosphatidyl inositol (Ptdlns) turnover are examined in MCF-7 human breast cancer cells in response to estradiol treatment. Elevated levels of Ptdlns are observed 12-24 h after estradiol treatment, occur at estradiol concentrations as low as 10-12 m, and are competitively blocked by the antiestrogen LY117018. MCF-7 cells secrete a transforming growth factor (TGF) α-like material which can partly replace estradiol in conferring tumorgen-icity in nude mice. We show that acute or chronic treatment of MCF-7 cells with TGFα results in elevated Ptdlns turnover and that chronic treatment increases growth rate. In contrast TGFβ is growth inhibitory and blocks estradiol-induced increases in Ptdlns turnover. A phosphatidyl inositol 4, 5-bisphos-phate specific phospholipase-C activity has been identified and is elevated in association with estradiol treatment. These data are consistent with estradiol-induced autocrine growth factors, including TGFα, acting through the Ptdlns turnover pathway as part of their mechanism of action.

Original languageEnglish (US)
Pages (from-to)159-166
Number of pages8
JournalMolecular Endocrinology
Volume2
Issue number2
DOIs
StatePublished - Aug 1988

ASJC Scopus subject areas

  • Molecular Biology
  • Endocrinology

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