Modulation of c-myc expression by beta interferon in human breast and prostate cancer cells

Altered expression of thec-myc oncogene has been associated with both etiology and differentiation of a wide variety of malignancies. In view of the demonstrated ability of interferon (IFN) to inhibit celll growth and to induce cell differentiation, as indicated by the enhancement of steroid hormone receptor level in human breast and prostatic cancer cell lines, we studied the effect of recombinant beta-interferon (rβ-IFN) on c-myc encodedp67 protein in an estrogen-sensitive (CG-5) and in an estrogen-insentive (MDA-MB-231) breast cancer cell line. In prostatic hormone-insensitive cancer cells (PC-3), c-myc expression was investigated at the mRNA level after natural beta-interferon (β-IFN) treatment. The 3 cell lines are sensitive to the antiproliferative action of IFN (10-100 IU/ml), particularly after 6 days of treatment. In CG-5 cells, p67 was consistently reduced after 120-168 hours of rβ-IFN (1000 IU/ml) treatment. In the same experimental conditions no effect was observed in MDA-MB-453 cells. In PC-3 cells c-myc mRNA was decreased by β-IFN 810-1000 IU/ml) after 2 hours and this effect was evident until 12 hours (10 IU/ml). Our data indicate that rβ-IFN and β-IFN are able to induce a substantial decrement of c-myc expression even if this effect seems, in CG-5 cells, to be not related to the antiproliferative activity of the cytokine.