Inhibition of insulin-like growth factor-I responses in MCF-7 cells by 2,3,7,8-tetrachlorodibenzo-p-dioxin and related compounds
| Autor: | Stephen Safe, L. Biegel, C. Rowlands, H. Liu, T.R. Narasimhan |
|---|---|
| Rok vydání: | 1992 |
| Předmět: |
medicine.medical_specialty
Polychlorinated Dibenzodioxins Receptors Drug medicine.medical_treatment Breast Neoplasms Biology Biochemistry Receptor IGF Type 1 Insulin-like growth factor chemistry.chemical_compound Endocrinology Internal medicine Tumor Cells Cultured medicine Humans Insulin-Like Growth Factor I Receptor Molecular Biology Benzofurans Estradiol Cell growth Growth factor Somatomedin Receptors Aryl Hydrocarbon MCF-7 chemistry Cancer cell Thymidine Cell Division |
| Zdroj: | Molecular and Cellular Endocrinology. 87:19-28 |
| ISSN: | 0303-7207 |
| DOI: | 10.1016/0303-7207(92)90229-y |
| Popis: | Insulin-like growth factor-I (IGF-I) stimulated the growth and [3H]thymidine uptake in MCF-7 human breast cancer cells grown in serum- and growth factor-inactivated serum-containing media. Cotreatment of the cells with IGF-I plus 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) resulted in a significant decrease in mitogen-induced cell proliferation and [3H]thymidine uptake. Similar effects were observed for cells treated with 2,3,7,8-TCDD and IGF-I plus 17 beta-estradiol. The relative antimitogenic activities of 2,3,7,8-TCDD and related compounds followed the order 2,3,7,8-TCDD greater than 2,3,7,8-tetrachlorodibenzofuran (TCDF) greater than 1,2,7,8-TCDF greater than 1,3,7,8-TCDD which was similar to their aryl hydrocarbon (Ah) receptor binding affinities. The results showed that 2,3,7,8-TCDD did not alter the IGF-I receptor mRNA levels or the KD values for binding of [125I]IGF-I to the IGF-I receptor in MCF-7 cells. However, 2,3,7,8-TCDD significantly decreased the number of IGF-I-induced IGF-I receptor binding sites and this may play a role in the growth-inhibitory properties of 2,3,7,8-TCDD and related compounds and in the 'cross-talk' between the two endocrine-response pathways. |
| Databáze: | OpenAIRE |
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