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Calcified Tissue International

, Volume 60, Issue 6, pp 513–519 | Cite as

Regulation of c-fos and c-jun Expression by Calcitonin in Human Breast Cancer Cells

  • M.  Lacroix
  • J. J.  Body
Article

Abstract.

Breast cancer cells (BCC) have calcitonin (CT) receptors, yet the action of the hormone on these cells is largely unknown. We found that CT produced a strong and transient time- and dose-dependent increase in c-fos mRNA in BCC lines. This event was prevented by a protein kinase A (PKA) inhibitor, H89. CT alone did not influence the expression of c-jun and of the tissue inhibitors of metalloproteases (timp) -1 and -2 mRNAs; however, it reduced the induction of these mRNAs by the protein kinase C (PKC) activator phorbol 12-myristate 13-acetate (PMA), without apparent changes in the half-life of the mRNA (measured for c-jun). Along the same line, CT reduced the c-jun induction and T-47D growth stimulation by epidermal growth factor (EGF) and insulin. These effects were mimicked by forskolin and/or prevented by H89, suggesting that PKA activation was involved. These results indicate that CT modulates in BCC the mRNA levels of two important growth-related early response genes (c-fos and c-jun) and of two other genes (timp-1 and -2) involved in the control of metastatic events.

Key words

Calcitonin — Breast cancer —c-fos—c-jun— Cell growth. 

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Copyright information

© Springer-Verlag New York Inc. 1997

Authors and Affiliations

  • M.  Lacroix
    • 1
  • J. J.  Body
    • 1
  1. 1.Bone Metabolism Unit, Service de Médecine et Laboratoire d'Investigation Clinique H. J. Tagnon, Institut J. Bordet, rue Héger-Bordet 1, Université Libre de BruxellesB-1000 BrusselsBelgium

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