Specific glucocorticoid binding in human hemopoietic cell lines and neoplastic tissue.

摘要: Summary Triamcinolone acetonide-3H (TA-3H) binding to subcellular macromolecular fractions was studied in three human lymphoid cell lines (HRIK, RPMI 8226, and MOLT-4), four lymphosarcomatous tumors, leukemic leukocytes obtained from the peripheral blood of patients with acute lymphocytic leukemia, six myelocytic eight chronic two leukemia. Specific binding, which manifested by a high affinity TA-3H greater inhibition this cortisol, compared that inactive steroid epicortisol, found lines, tissue, leukemia cells, cells. Sedimentation coefficients “S” complex were one tumors. When cells incubated at 0°, extraction low-salt buffer produced 6.5 S complex, while high-salt 4 complex. After incubation 37°, yielded only small amount sedimenting S. However, extracted 27,000 × g pellet extract, suggesting 37° resulted movement into nucleus. Incubation HRIK presence 10-5 10-4m cortisol 22.5 50% uridine-3H uptake incorporation cellular RNA inhibited after cortisol. The relative insensitivity these despite their specific-binding capacity, indicate factors other than play an important role determining sensitivity glucocorticoid action.