Retinoic acid or methionine enhance interferon's inhibition of the transformed phenotype with no effect on tumorigenicity.
Retinoic acid (RA) and methionine were studied for their relative effectiveness in enhancing the ability of interferons (IFNs) to reverse the phenotype of murine methylcholanthrene (MCA)-transformed cells and human osteosarcoma (OHA) cells. Treatment with RA (1 microM) and methionine (25mM) alone had minimal or no effect on the proliferation of MCA and OHA cells or on the ability to form tumors in animals. Combination of these two agents with IFNs however, potentiated the inhibitory effects of IFNs on proliferation and colony formation of MCA transformed cells but not on their tumorigenicity. Similarly in human tumor OHA cells, only the combination of IFN and RA was more effective than IFN alone on proliferation and colony formation but not on tumorigenicity. Thus, the enhanced effects of combined treatments on cell proliferation in vitro could be distinguished from the inhibitory effects of IFNs on tumorigenicity in both murine transformed cells and human tumor cells.
Brouty-Boyé
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Laboratoire d'Oncologie Virale, Institut de Recherches Scientifiques sur le Cancer, Villejuif, France.
Lejealle
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R
D000818:Animals; D015197:Carcinogenicity Tests; D002455:Cell Division / Q000187:drug effects; D003114:Colony-Forming Units Assay; D003131:Combined Modality Therapy; D006801:Humans; D007370:Interferon Type I / Q000494:pharmacology*; D008715:Methionine / Q000494:pharmacology*; D008748:Methylcholanthrene / Q000633:toxicity; D051379:Mice; D010641:Phenotype; D014212:Tretinoin / Q000494:pharmacology*; D014407:Tumor Cells, Cultured
D007370:Interferon Type I; D008748:Methylcholanthrene; D014212:Tretinoin; D008715:Methionine