Abstract
Interferon exerts, in addition to its well recognized antiviral activity, an antiproliferative effect1,2 and has been found to reduce plasminogen activator secretion3, to re-establish contact inhibition4 and to inhibit the growth in semi-solid agar5 of neoplastic cells. Double-stranded RNA (dsRNA) is both an interferon inducer and an activator of two interf eron-induced enzymes, a protein kinase and a 2′,5′ oligoadenylate synthetase6. However, the molecular bases for the antiproliferative and antineoplastic effects of interferon, and their relationship to dsRNA, are unknown. We have now characterized the antiproliferative effects of interferon and dsRNA on the human HT1080 fibrosarcoma7 and RT4 epidermal carcinoma8 cell lines. Luria-Delbrück fluctuation analysis9 of interferon resistance indicates that the resistance trait is a non-randomly acquired phenotype which was probably induced by interferon at the time of selection. The interferon-resistant (IFNr) cells retained sensitivity to the antiviral effects of interferon, as well as to the antiproliferative effects of dsRNA.
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Lin, S., Greene, J., Ts'o, P. et al. Sensitivity and resistance of human tumour cells to interferon rIn ·rCn. Nature 297, 417–419 (1982). https://doi.org/10.1038/297417a0
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DOI: https://doi.org/10.1038/297417a0
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