cis- and trans-Acting Genetic Elements Responsible for Induction of Specific Genes by Tumor Promoters, Serum Factors, and Stress

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Abstract
Exposure of mammalian cells to adverse environmental conditions triggers the onset of specific genetic responses, which are likely to have evolved as mechanisms that protect the cell against insult. This occurs by the rapid induction of sets of genes whose products are supposed to exert a protective effect upon the cell. The spectrum of genes that are turned on during a response to environmental stress depends on the particular type of insult. Thus, elevated temperature leads to induction of heat shock proteins that are thought to allow cells to withstand such a condition (see Ref. 1 for a review); exposure to toxic heavy metal ions, such as cadmium and mercury, leads to induction of metallothioneins (MTs), which are low molecular weight, cysteine-rich, heavy metal-binding proteins (see Ref. 2 for a review); and exposure to ultraviolet (UV) irradiation and other deoxyribonucleic acid (DNA)-damaging agents triggers a response known as the UV response whose putative role is to protect cells against DNA damage [3,4]. Interestingly, the activation of the UV response leads to the induction of gene products whose role in DNA repair is not obvious at this point, but some of which are likely to be involved in tumor promotion, a known consequence of DNA damage (see Ref. 5 for a review). The relationships between the UV response and tumor promotion will be discussed below. While 416each of these responses involves the induction of a distinct set of proteins, there also is some overlap between them. For example, exposure to toxic doses of cadmium and copper also triggers induction of heat shock proteins (see Ref. 6 and references therein), and to UV or mitomycin C leads to induction of MT genes [7]. However, heat shock does not induce MTs, and exposure to DNA damage does not elicit the heat shock response.

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