GammaInterferon Regulates LongTerminal Repeat-Controlled Oncogene Expression inTransformed MouseFibroblasts atthe LevelofmRNA Transcription

activity incells transformed withthecatgeneunderthe control oflongterminal repeats. Interferons (IFNs) areagroupofrelated cytokines with multiple biological activities, someofwhich, e.g., cytostatic action orinduction ofdifferentiation oftumorcells, may contribute tothecontrol ofmalignant disease (5,8,10,18, 23). frommodels ofoncogenic transformation offibroblasts, ithasbeenimplicated thatmodulation ofoncogene expressionisoneofthecrucial mechanisms ofantitumoral activities ofIFNs(5,7,12,13,19,20,21), although nogeneral rules haveemerged astothemechanisms bywhichIFNs exert control ofoncogene expression. Using NIH3T3cells transformed byoncogenes ofdifferent transforming capacity, we studied themechanisms ofgammaIFN-mediated inhibition oflongterminal repeat (LTR)-controlled oncogene expression. Thedatashowthat murine recombinant gamma IFN(mu-rIFN-gamma) downregulates theexpression of v-Ha-ras, v-mos, andc-myconcogenes atthetranscriptional level andcauses phenotypical reversion ofv-mosandc-myc butnotofv-Ha-ras transformants. Oncogene-mediated