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Involvement of fos in spontaneous and ultraviolet light‐induced genetic changes
Author(s) -
van den Berg Susanne,
Kaina Bernd,
Rahmsdorf Hans J.,
Ponta Helmut,
Herrlich Peter
Publication year - 1991
Publication title -
molecular carcinogenesis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.254
H-Index - 97
eISSN - 1098-2744
pISSN - 0899-1987
DOI - 10.1002/mc.2940040609
Subject(s) - biology , tumor promotion , ultraviolet light , mutagenesis , microbiology and biotechnology , gene , oncogene , transcription (linguistics) , transcription factor , cancer research , mutation , genetics , carcinogenesis , cell cycle , linguistics , chemistry , philosophy , photochemistry
Transient overexpression of ras, mos, or fos transcribed from various inducible promoters in NIH 3T3 cells causes significant increases in the frequency of chromosomal aberrations and, as shown for fos, in gene mutations. Under the experimental conditions of exponential growth and full serum supply, overexpression of the oncogenes does not increase the proliferation rate of cells. The generation of ras‐ and mos‐induced chromosomal aberrations was suppressed in cells that had been deprived of fos protein by antisense c‐ fos oligodeoxynucleotides. The induction of chromosomal aberrations by ultraviolet irradiation is also suppressed by antisense c‐ fos oligodeoxynucleotides. The data suggest that fos protein alone, or a transcription factor that contains fos protein as a subunit, activates or induces the synthesis of one or several mutator functions. Oncogenedriven mutagenesis could account for the accumulation of additional mutations after the activation of an oncogene, which may furnish a mechanistic basis for tumor promotion and tumor progression.