Biochemical correlates of phenotypic reversion in interferon-treated mouse cells transformed by a human oncogene.
Mouse interferon (IFN) induced a phenotypic reversion in RS 485, a clonal line of NIH 3T3 oncogenically transformed by a human c-Ha-rasl gene activated by Ha-MuSV long terminal repeats (LTRs). Transfected c-Ha-ras DNA, unchanged in quantity and distribution, as compared to the parental RS 485 transformed cells, was still present in these revertants; however, there was a significant reduction in the amount of c-Ha-ras specific mRNA and of c-Ha-ras specified p21 protein.
D000818:Animals; D002460:Cell Line; D002471:Cell Transformation, Neoplastic / Q000378:metabolism / Q000473:pathology*; D002999:Clone Cells / Q000032:analysis; D004247:DNA / Q000378:metabolism; D006801:Humans; D007163:Immunosorbent Techniques; D007372:Interferons / Q000494:pharmacology*; D051379:Mice; D009363:Neoplasm Proteins / Q000378:metabolism; D009693:Nucleic Acid Hybridization; D009857:Oncogenes; D016283:Proto-Oncogene Proteins p21(ras); D012333:RNA, Messenger / Q000378:metabolism
D009363:Neoplasm Proteins; D012333:RNA, Messenger; D004247:DNA; D007372:Interferons; C501009:HRAS protein, human; D016283:Proto-Oncogene Proteins p21(ras)