The large group of steroid, retinoic acid (retinoid), and thyroid hormones exert at least part of their effects by a mechanism fundamentally different from that of other hormones: they act in the nucleus to alter gene expression. We therefore discuss their mode of action in detail in Chapter 28, along with other mechanisms for regulating gene expression. Here we give a brief overview.
Steroid hormones (estrogen, progesterone, and cortisol, for example), too hydrophobic to dissolve readily in the blood, are carried on specific carrier proteins from their point of release to their target tissues. In target cells, these hormones pass through the plasma membranes by simple diffusion and bind to specific receptor proteins in the nucleus (Fig. 12-40). Hormone binding triggers changes in the conformation of the receptor proteins so that they become capable of interacting with specific regulatory sequences in DNA called hormone response elements (HREs), thus altering gene expression (see Fig. 28-31). The bound receptor-hormone complex can either enhance or suppress the expression of specific genes adjacent to HREs. Hours or days are required for these regulators to have their full effect— the time required for the changes in RNA synthesis and subsequent protein synthesis to become evident in altered metabolism.
The specificity of the steroid-receptor interaction is exploited in the use of the drug tamox-ifen to treat breast cancer. In some types of breast cancer, division of the cancerous cells depends on the continued presence of the hormone estrogen. Tamox-ifen competes with estrogen for binding to the estrogen receptor, but the tamoxifen-receptor complex has little or no effect on gene expression; tamoxifen is an antagonist of estrogen. Consequently, tamoxifen administered after surgery or during chemotherapy for hormone-dependent breast cancer slows or stops the growth of remaining cancerous cells.
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