Title |
Regulation of c-fos and c-jun Expression by Calcitonin in Human Breast Cancer Cells
|
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Published in |
Calcified Tissue International, July 1997
|
DOI | 10.1007/s002239900273 |
Pubmed ID | |
Authors |
M. Lacroix, J. J. Body |
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. |
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Geographical breakdown
Country | Count | As % |
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Unknown | 5 | 100% |
Demographic breakdown
Readers by professional status | Count | As % |
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Professor | 3 | 60% |
Student > Master | 1 | 20% |
Unknown | 1 | 20% |
Readers by discipline | Count | As % |
---|---|---|
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Social Sciences | 1 | 20% |
Agricultural and Biological Sciences | 1 | 20% |
Unknown | 1 | 20% |