Key result
Interferon alpha suppresses cell proliferation without requiring c-myc mRNA reduction.
Why the study?
The relationship between interferon modulation of c-myc expression and the phenotype of interferon resistance in Daudi cells was unclear.
The reduction of c-myc mRNA may not be a prerequisite for the inhibition of cell proliferation in interferon-treated Burkitt lymphoma cells.
Questions c-myc downregulation as prerequisite for interferon antiproliferative effects in lymphoma cells; leaves open alternative pathways for validation.
Treatment of interferon-sensitive Daudi cell with electrophoretically pure human interferon alpha markedly reduced the level of c-myc mRNA, increased the level of class I histocompatibility antigen (HLA) mRNA, and did not affect the level of actin mRNA within the same cells. In contrast, the level of c-myc mRNA or HLA mRNA did not change significantly following interferon treatment in different clones of Daudi cells selected for resistance to the antiproliferative action of interferon. These cells possessed interferon receptors, however, and responded to interferon modulation of other genes, including 2',5' oligoisoadenylate synthetase (M. G. Tovey, M. Dron, K. E. Mogensen, B. Lebleu, N. Metchi, and J. Begon-Lours, Guymarho, J. Gen. Virol., 64:2649-2653, 1983; M. Dron, M. G. Tovey, and P. Eid, J. Gen. Virol., 66:787-795, 1985). A clone of interferon-resistant Daudi cells which had reverted to almost complete sensitivity to both the antiproliferative action of interferon and the interferon-enhanced expression of HLA mRNA remained refractory, however, to interferon modulation of c-myc expression, suggesting that a reduced level of c-myc mRNA may not be a prerequisite for inhibition of cell proliferation in interferon-treated cells. Our results do not exclude the possibility, however, that posttranscriptional modification(s) of c-myc expression may precede an inhibition of cell proliferation in interferon-treated cells.
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Dron et al. (1986) studied Burkitt lymphoma-derived Daudi cells. Human interferon alpha vs. Untreated cells was evaluated on c-myc mRNA level and cell proliferation. Human interferon alpha markedly reduced c-myc mRNA levels in sensitive Daudi cells but not in an interferon-sensitive revertant clone, suggesting reduced c-myc mRNA may not be a prerequisite for the antiproliferative action of interferon.
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