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Role of estrogen-induced insulin-like growth factors in the proliferation of human breast cancer cells.
Cancer Res. 1990 Dec 15; 50(24):7770-4.CR

Abstract

Insulin-like growth factor I (IGF-I) is the most potent growth factor for estrogen (E2)-dependent breast cancer cell lines. It has been reported that such cell lines produce an immunoreactive IGF-I-related protein in an E2-dependent fashion, while autonomously growing cell lines constitutively produce these factors, indicating that they might be involved in autocrine growth stimulation of breast cancer cells. We have studied the role of IGFs in autocrine growth stimulation of the E2-dependent breast cancer cell line MCF7 by using IGF-binding proteins (BPs) that were able to neutralize completely the mitogenic effect of IGF-I on this cell line. These BPs, however, did not have any inhibitory effect on E2-induced mitogenesis, suggesting that secretion of autocrine IGFs is not involved in growth stimulation by E2. To exclude the possibility that variants of IGF are produced by the cells that are not recognized by the BPs, we also studied the production of biologically active IGF using the same MCF7 cell line in a sensitive bioassay in which the various forms of IGF and insulin can be detected. Although the conditioned medium (CM) of human fibroblasts used as a control showed IGF-like activity in this assay, no such activity was detected in CM of both untreated and E2-stimulated MCF7 cells, while the CM of the E2-independent cell lines BT20 and Hs578T had only slight mitogenic activity or was even growth inhibitory, respectively. These data show that no significant secretion of biologically active IGFs by human breast cancer cells could be detected and do not support a possible autocrine function of IGFs in the proliferation of such cells. Because E2-dependent cells strongly react to externally added IGF-like factors produced by human fibroblasts, a role for IGFs in paracrine regulation of proliferation is suggested.

Authors+Show Affiliations

Hubrecht Laboratory, Netherlands Institute for Developmental Biology, Utrecht.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

2174732

Citation

van der Burg, B, et al. "Role of Estrogen-induced Insulin-like Growth Factors in the Proliferation of Human Breast Cancer Cells." Cancer Research, vol. 50, no. 24, 1990, pp. 7770-4.
van der Burg B, Isbrücker L, van Selm-Miltenburg AJ, et al. Role of estrogen-induced insulin-like growth factors in the proliferation of human breast cancer cells. Cancer Res. 1990;50(24):7770-4.
van der Burg, B., Isbrücker, L., van Selm-Miltenburg, A. J., de Laat, S. W., & van Zoelen, E. J. (1990). Role of estrogen-induced insulin-like growth factors in the proliferation of human breast cancer cells. Cancer Research, 50(24), 7770-4.
van der Burg B, et al. Role of Estrogen-induced Insulin-like Growth Factors in the Proliferation of Human Breast Cancer Cells. Cancer Res. 1990 Dec 15;50(24):7770-4. PubMed PMID: 2174732.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Role of estrogen-induced insulin-like growth factors in the proliferation of human breast cancer cells. AU - van der Burg,B, AU - Isbrücker,L, AU - van Selm-Miltenburg,A J, AU - de Laat,S W, AU - van Zoelen,E J, PY - 1990/12/15/pubmed PY - 1990/12/15/medline PY - 1990/12/15/entrez SP - 7770 EP - 4 JF - Cancer research JO - Cancer Res. VL - 50 IS - 24 N2 - Insulin-like growth factor I (IGF-I) is the most potent growth factor for estrogen (E2)-dependent breast cancer cell lines. It has been reported that such cell lines produce an immunoreactive IGF-I-related protein in an E2-dependent fashion, while autonomously growing cell lines constitutively produce these factors, indicating that they might be involved in autocrine growth stimulation of breast cancer cells. We have studied the role of IGFs in autocrine growth stimulation of the E2-dependent breast cancer cell line MCF7 by using IGF-binding proteins (BPs) that were able to neutralize completely the mitogenic effect of IGF-I on this cell line. These BPs, however, did not have any inhibitory effect on E2-induced mitogenesis, suggesting that secretion of autocrine IGFs is not involved in growth stimulation by E2. To exclude the possibility that variants of IGF are produced by the cells that are not recognized by the BPs, we also studied the production of biologically active IGF using the same MCF7 cell line in a sensitive bioassay in which the various forms of IGF and insulin can be detected. Although the conditioned medium (CM) of human fibroblasts used as a control showed IGF-like activity in this assay, no such activity was detected in CM of both untreated and E2-stimulated MCF7 cells, while the CM of the E2-independent cell lines BT20 and Hs578T had only slight mitogenic activity or was even growth inhibitory, respectively. These data show that no significant secretion of biologically active IGFs by human breast cancer cells could be detected and do not support a possible autocrine function of IGFs in the proliferation of such cells. Because E2-dependent cells strongly react to externally added IGF-like factors produced by human fibroblasts, a role for IGFs in paracrine regulation of proliferation is suggested. SN - 0008-5472 UR - https://www.unboundmedicine.com/medline/citation/2174732/Role_of_estrogen_induced_insulin_like_growth_factors_in_the_proliferation_of_human_breast_cancer_cells_ L2 - http://cancerres.aacrjournals.org/cgi/pmidlookup?view=long&pmid=2174732 DB - PRIME DP - Unbound Medicine ER -