The molecular mechanisms underlying the growth inhibition induced by interferon-α (IFN-α) in B16 murine melanoma cells were investigated. IFN-α did not induce cell apoptosis, but strongly interfered with the synthesis of basic fibroblast growth factor (bFGF), which acts as an autocrine growth factor in this system. Inhibition of bFGF synthesis was observed at the same concentrations (50-500 pM, 10-100 U/ml) of IFN-α able to induce growth arrest of B16 melanoma cells. Although the synthesis of acidic (a)FGF was only slightly affected by IFN-α, the cytokine induced release of an aFGF-related low-molecular-weight peptide, which was able to interfere with bFGF binding to surface receptors. Thus, the molecular mechanisms of IFN-α activity on melanoma cells include a specific modulation of the bFGF autocrine circuit.
|Number of pages||7|
|Journal||Biochemical and Biophysical Research Communications|
|Publication status||Published - Sep 7 1999|
ASJC Scopus subject areas
- Molecular Biology