Radiotoxicity of 17α-[125I]iodovinyl-11β-methoxyestradiol in MCF-7 human breast cancer cells
Autor: | Michael W. Epperly, William D. Bloomer, K.M.R. Pillai, W. H. McLaughlin, Kalyani M. Damodaran |
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Rok vydání: | 1991 |
Předmět: |
medicine.medical_specialty
Cell Survival medicine.drug_class Endocrinology Diabetes and Metabolism Clinical Biochemistry Breast Neoplasms Biology Binding Competitive Biochemistry Cell Line Iodine Radioisotopes Endocrinology Internal medicine medicine Humans Cytotoxic T cell Molecular Biology Estradiol Estrogen receptor binding Cancer Biological Transport Cell Biology medicine.disease In vitro Kinetics Receptors Estrogen MCF-7 Cell culture Estrogen Cancer cell Cancer research Molecular Medicine Female |
Zdroj: | The Journal of Steroid Biochemistry and Molecular Biology. 39:729-734 |
ISSN: | 0960-0760 |
DOI: | 10.1016/0960-0760(91)90373-d |
Popis: | Therapeutic strategies for human breast cancer using 125I-labeled steroid hormones are clinically attractive in light of the estrogen dependence of many human breast cancers and the favorable microdosimetry resulting from 125I decay. We determined the uptake specific estrogen receptor binding and radiotoxicity of 17 alpha-[125I]iodovinyl-11 beta-methoxyestradiol (125IVME2) in vitro using cultured MCF-7 human breast carcinoma cells. 125IVME2 rapidly enters MCF-7 cells and reaches a plateau in the presence of competing 10(-7) M 17 beta-estradiol. In the absence of competitor, uptake is substantially greater before reaching a plateau. Efflux of 125IVME2 from cells incubated in the absence of estradiol decreases to levels corresponding to specific binding. Under equilibrium conditions and in the absence of competitor, 125IVME2 binds to both specific and nonspecific sites but, in the presence of excess 17 beta-estradiol, the observed binding is nonspecific. 125IVME2 is cytotoxic to exponentially growing MCF-7 cells and produces a survival curve typical of those observed for [125I]iododeoxyuridine and 16 alpha-[125I]iodoestradiol. |
Databáze: | OpenAIRE |
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