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How do steroid drugs change gene expression in a cell nucleus?

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Gleevec; imatinib — drug Docking of the anticancer drug Gleevec (imatinib) in the abl domain of the bcr-abl tyrosine kinase. Abnormalities in bcr-abl stimulate the continuous proliferation of bone marrow stem cells, causing an increase in myelogenous cells (granulocytes and macrophages) in the body and leading to chronic myelogenous leukemia (CML).

Steroid drugs change gene expression by acting directly within the cell nucleus, a process that distinguishes them from many other chemical agents that bind to receptors on the cell surface.1

Because steroids are capable of crossing the cell membrane, they can enter the cytoplasm and bind to specific intracellular receptors. Once the steroid binds to its receptor, the resulting drug-receptor complex migrates into the cell nucleus. Inside the nucleus, this complex interacts with specific regions of deoxyribonucleic acid (DNA).12

By binding to these genetic sequences, the complex acts to activate or repress transcription, which is the initial step in protein biosynthesis. This interaction ultimately alters the rate at which specific proteins are synthesized—increasing the production of some while decreasing the production of others. Because this mechanism involves complex intracellular migration and direct interaction with genetic material, steroid-mediated effects typically occur much more slowly than those triggered by membrane-bound receptors, often taking hours or days to manifest.21