Dissociation of thymidine incorporation and transferrin receptor expression from cell growth and c-myc accumulation in α-interferon-treated cells
α-Interferon is capable of altering the pattern of growth of both normal and neoplastic cells, but the pathways essential to sensitivity and resistance to α-interferon are unknown. To explore the growth inhibition induced by α-interferon, we examined the interferon-sensitive cell line Daudi and the resistant cell line HL-60. In Daudi, α-interferon induced a fall in c-myc mRNA accumulation at 24 h, inhibited tritiated thymidine ([3H]Thd) uptake at 48-72 h, and inhibited proliferation at 72-96 h. The half-life of c-myc mRNA was shortened from 31 to 13 min by α-interferon treatment. In HL-60, no alteration in c-myc accumulation or cell growth was observed, but [3H]Thd uptake was inhibited by 49%. Exogenous thymidine partially reversed the effects of α-interferon on [3H]Thd incorporation. The number of transferrin receptors, as measured by immunofluorescence, was unaffected by α-interferon in both cell lines. We conclude that the growth inhibitory effects of α-interferon are neither dependent upon inhibition of thymidine metabolism nor on expression of the transferrin receptor, but may be linked to control of c-myc.
Meadows, LM; George, DJ; Kaufman, RE
Journal of Biological Response Modifiers
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