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STUDIES ON THE MECHANISM OF THE ANTIPROLIFERATIVE EFFECT OF INTERFERON

A number of in vitro and in vivo studies have indicated that cellular proliferation is inhibited after treatment with interferon (IFN) . We have undertaken studies to determine the molecular basis for the direct effect of interferon on cell growth. In order to distinguish effectively alterations in cell proliferation from other IFN-induced changes, we have established a series of Friend erythroleukemia cell clones resistant to growth inhibition by interferon in vitro. These mutants were selected by continuous passage in 5000 units/ml of purified mouse fibroblast interferon (8.4 X lo7 U/mg protein). Clones isolated from IFNcontaining methylcellulose were grown in the absence of interferon and then screened for proliferation in the presence and absence of IFN. The clones were concomitantly tested for the production of retrovirus particles by assay of reverse transcriptase in the culture medium. Results with a representative group of clones are shown in TABLE 1. Three classes of clones were isolated: resistant, sensitive, and a single clone, F4-6 R-301, which proliferates more rapidly in the presence of IFN. Analysis of reverse-transcriptase-containing particles indicated a 100% correlation between the release of virus particles and whether the clone was growth-inhibited or -stimulated by IFN. Cell lines sensitive to growth inhibition by IFN varied in the extent of inhibition of virus release. In some cases (such as F4-6 R-302) virus release as measured by reverse transcriptase was inhibited to a greater degree than cell growth. Whether differences in sensitivity to the inhibition of virus release relates to the rapidity of the growth response to IFN is under study. We have used RNA tumor virus proteins as probes for interferon-induced alterations in protein synthesis, modification, and secretion.