TY - JOUR
T1 - Inhibition of insulin-like growth factor-I responses in MCF-7 cells by 2,3,7,8-tetrachlorodibenzo-p-dioxin and related compounds
AU - Liu, H.
AU - Biegel, L.
AU - Narasimhan, T. R.
AU - Rowlands, C.
AU - Safe, S.
N1 - Funding Information:
The financial assistance of the National Institutes of Health (ES041761 and the Texas Agricultural Experiment Station if gratefully acknowledged. S.S. is a Burroughs Wellcome Toxicology Scholar.
Copyright:
Copyright 2014 Elsevier B.V., All rights reserved.
PY - 1992/9
Y1 - 1992/9
N2 - 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 17β-estradiol. The relative antimitogenic activities of 2,3,7,8-TCDD and related compounds followed the order 2,3,7,8-TCDD > 2,3,7,8-tetrachlorodi benzofuran (TCDF) > 1,2,7,8-TCDF > 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.
AB - 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 17β-estradiol. The relative antimitogenic activities of 2,3,7,8-TCDD and related compounds followed the order 2,3,7,8-TCDD > 2,3,7,8-tetrachlorodi benzofuran (TCDF) > 1,2,7,8-TCDF > 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.
KW - Inhibition by 2,3,7,8-tetrachlorodibenzo-p-dioxin
KW - Insulin-like growth factor-I-induced growth
KW - MCF-7 cell
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U2 - 10.1016/0303-7207(92)90229-Y
DO - 10.1016/0303-7207(92)90229-Y
M3 - Article
C2 - 1332906
AN - SCOPUS:0026674353
SN - 0303-7207
VL - 87
SP - 19
EP - 28
JO - Molecular and cellular endocrinology
JF - Molecular and cellular endocrinology
IS - 1-3
ER -