Carcinogen-induced trans activation of gene expression.
We report a new mechanism of carcinogen action by which the expression of several genes was concomitantly enhanced. This mechanism involved the altered activity of cellular factors which modulate the expression of genes under their control. The increased expression was regulated at least in part on the transcriptional level and did not require amplification of the overexpressed genes. This phenomenon was transient; it was apparent as early as 24 h after carcinogen treatment and declined a few days later.
Kleinberger
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Department of Microbiology, George S. Wise Faculty of Life Sciences, Tel Aviv University, Ramat Aviv, Israel.
Flint
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YB
Blank
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Etkin
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Lavi
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D015127:9,10-Dimethyl-1,2-benzanthracene / Q000494:pharmacology; D000123:Acetyltransferases / Q000235:genetics / Q000378:metabolism; D000199:Actins / Q000096:biosynthesis / Q000235:genetics; D000818:Animals; D000957:Antigens, Viral, Tumor / Q000096:biosynthesis / Q000235:genetics; D016590:Aphidicolin; D002273:Carcinogens / Q000494:pharmacology*; D002461:Cell Line, Transformed; D015500:Chloramphenicol O-Acetyltransferase; D004224:Diterpenes / Q000494:pharmacology; D005784:Gene Amplification; D005786:Gene Expression Regulation / Q000187:drug effects*; D008769:Methylnitronitrosoguanidine / Q000494:pharmacology; D013539:Simian virus 40; D014158:Transcription, Genetic / Q000187:drug effects*; D014162:Transfection
D000199:Actins; D000957:Antigens, Viral, Tumor; D002273:Carcinogens; D004224:Diterpenes; D008769:Methylnitronitrosoguanidine; D016590:Aphidicolin; D015127:9,10-Dimethyl-1,2-benzanthracene; D000123:Acetyltransferases; D015500:Chloramphenicol O-Acetyltransferase