Abstract
Two fundamental concepts concerning the actions of steroid hormones seem to be generally agreed upon. The first is that steroids are inducers, inducers of various specific macromolecules in appropriate target cells. To cite but a few examples, in liver and in certain cultured hepatoma cells, glucocorticoids induce increased synthesis of specific enzymes, such as tryptophan oxygenase and tyrosine aminotransferase (1–3). In immature chicks, estrogens provoke growth, as well as increased specific RNA and protein synthesis (ovalbumin) in target cells (4,5). In rat uterus overall increased growth and specific protein synthesis are induced by estrogen (4,5). Dihydrotestosterone induces several enzymes in rat kidney (6), and progesterone induces avidin in estrogen-primed chick oviduct (7). The list is long (8), and the point seems clear. Steroids are inducers of proteins, DNA, and all the various major classes of RNA. Not all effects are seen in all tissues, of course. The differentiated nature of various cell types defines whether they respond at all to steroids, and if so, to which steroids with which responses. The elements responsible for such specificity and differentiation raise the second fundamental concept in steroid hormone action.
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Thompson, E.B. (1976). The Cellular Actions of Glucocorticoids in Relation to Human Neoplasms. In: Menon, K.M.J., Reel, J.R. (eds) Steroid Hormone Action and Cancer. Current Topics in Molecular Endocrinology, vol 4. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-2601-4_10
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