Defects of TGF-beta receptor signaling in mammary cell tumorigenesis.

M. G. Brattain, Y. Ko, S. S. Banerji, G. Wu, J. K. Willson

Research output: Contribution to journalReview article

24 Scopus citations

Abstract

Transforming growth factor beta (TGF-beta) receptor expression and signal transduction in human breast cancer are reviewed as a function of estrogen receptor (ER) expression. ER+ breast cancer cells are generally resistant to the inhibitory effects of TGF-beta. The only known exception appears to be MCF-7 early passage cells which are initially sensitive to TGF-beta, but gain resistance after long-term passage in tissue culture. A number of studies have shown that loss of sensitivity is due to inadequate TGF-beta type II (TGFRII) receptor expression. Stable transfection of TGFRII into ER+ breast cancer cell lines results in the acquisition of TGF-beta sensitivity and reversion of malignancy. Although there are exceptions, ER- breast cancer cells usually express TGFRII, but nevertheless show a low level of sensitivity to TGF-beta. Thus resistance in these cells implies a postreceptor mechanism. Given the frequency with which loss of TGF-beta sensitivity has been associated with loss of TGFRII, the ER- breast cancer cell lines may represent valuable models for identifying postreceptor mechanisms of resistance.

Original languageEnglish (US)
Pages (from-to)365-372
Number of pages8
JournalJournal of mammary gland biology and neoplasia
Volume1
Issue number4
DOIs
StatePublished - Oct 1996
Externally publishedYes

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

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