Induction of jun Gene Family Members by Transforming Growth Factor a but not 17/3-Estradiol in Human Breast Cancer Cells

Nancy E. Davidson, Laura J. Prestigiacomo, Hillary A. Hahm

Research output: Contribution to journalArticlepeer-review


To investigate whether estrogen treatment of hormone-responsive human breast cancer cells was associated with activation of members of the jun family of immediate early response genes, the expression of these oncogenes in human breast cancer cells was examined. 17/3-Estradiol had little effect on expression of c-jun, jun B,jun D, or c-fos mRNA by MCF-7 cells over 12 h, although it stimulated c-myc expression 4-fold within 30 min. In contrast, several peptide growth factors, including transforming growth factor-α (TGF-α), rapidly and transiently induced expression of c-jun, jun B, and c-fos mRNA 4- to 10-fold over control. A similar pattern of expression was seen in two other estrogen-responsive human breast cancer cell lines, ZR-75-1 and T47D. Inhibition of protein synthesis by cycloheximide did not abrogate induction of c-jun or jun B mRNA by TGF-α in MCF-7 cells, suggesting that new protein synthesis was not required. In addition, nuclear runoff transcription analysis demonstrated that increased expression of c-jun and jun B mRNA after TGF-a treatment of MCF-7 cells was regulated at least in part at the transcriptional level. Chronic exposure of MCF-7 cells to 17β-estradiol for 24-48 h was associated with decreased expression of jun B mRNA only, while similar treatment with TGF-α did not change mRNA expression of any jun family member. Thus, expression of jun family members is induced by peptide growth factors like TGF-α but not 17β-estradiol in human breast cancer cells. These results suggest that these nuclear protooncogenes play different roles in modulating gene expression by MCF-7 cells after exposure to TGF-α or 17β-estradiol.

Original languageEnglish (US)
Pages (from-to)291-297
Number of pages7
JournalCancer Research
Issue number2
StatePublished - Jan 1993

ASJC Scopus subject areas

  • Oncology
  • Cancer Research


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