作者: Diane Bronzert , Karen Huff , Marc E. Lippman , C. Ronald Kahn , C. Kent Osborne
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摘要: We have examined the interaction of dexamethasone with ZR75-1 human breast cancer cell line to determine if glucocorticoids might directly inhibit growth cells. Growth these cells in serum-free medium was stimulated significantly by physiological concentrations insulin (0.1 1.0 nm). Pharmacological (10 nm) reduced number below that found controls and nearly abolished effect after several days culture. Thymidine uridine, but not leucine, incorporation into macromolecules or acetate fatty acids were similarly inhibited presence absence insulin. Dexamethasone did effects altering receptor affinity concentration, as determined Scatchard analyses binding. Net thymidine uptake trichloroacetic acid-soluble fraction dexamethasone. also kinase activity both control insulin-stimulated These data suggest multiple potential sites glucocorticoid action oppose They a direct inhibitory on proliferation cells, which may help explain tumor regression following pharmacological therapy.