Abstract
Glucocorticoids are widely used chemotherapeutic agents for multiple myeloma. Drug resistance to steroid therapies is associated with the downregulation or loss of glucocorticoid receptor expression in malignant plasma cells. In this study, we examined the constitutive expression of glucocorticoid receptor in dexamethasone-sensitive and dexamethasone-resistant multiple myeloma cell lines. We found that triptolide increased the amount of the phosphorylated glucocorticoid receptor and enhanced the growth inhibitory effect of dexamethasone. Notably, these effects could not be blocked by interleukin-6, one of the most important growth factors in multiple myeloma.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Antineoplastic Agents, Alkylating / pharmacology
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Cell Line, Tumor
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Dexamethasone / pharmacology
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Diterpenes / pharmacology*
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Drug Resistance, Neoplasm
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Epoxy Compounds / pharmacology
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Humans
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Interleukin-6 / pharmacology*
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Multiple Myeloma / drug therapy*
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Multiple Myeloma / metabolism
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Phenanthrenes / pharmacology*
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Phosphorylation / drug effects
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Receptors, Glucocorticoid / genetics*
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Receptors, Glucocorticoid / metabolism
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Up-Regulation / drug effects*
Substances
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Antineoplastic Agents, Alkylating
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Diterpenes
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Epoxy Compounds
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Interleukin-6
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Phenanthrenes
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Receptors, Glucocorticoid
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triptolide
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Dexamethasone