Insulin-Like Growth Factor-ll (IGF-II): A Potential Autocrine/Paracrine Growth Factor for Human Breast Cancer Acting via the IGF-I Receptor (original) (raw)

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1Department of Medicine, Division of Oncology, University of Texas Health Science Center San Antonio, Texas 78284; Laboratory of Molecular Endocrinology, University of California San Francisco, California 94143

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1Department of Medicine, Division of Oncology, University of Texas Health Science Center San Antonio, Texas 78284; Laboratory of Molecular Endocrinology, University of California San Francisco, California 94143

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1Department of Medicine, Division of Oncology, University of Texas Health Science Center San Antonio, Texas 78284; Laboratory of Molecular Endocrinology, University of California San Francisco, California 94143

Search for other works by this author on:

,

1Department of Medicine, Division of Oncology, University of Texas Health Science Center San Antonio, Texas 78284; Laboratory of Molecular Endocrinology, University of California San Francisco, California 94143

Search for other works by this author on:

,

1Department of Medicine, Division of Oncology, University of Texas Health Science Center San Antonio, Texas 78284; Laboratory of Molecular Endocrinology, University of California San Francisco, California 94143

Search for other works by this author on:

,

1Department of Medicine, Division of Oncology, University of Texas Health Science Center San Antonio, Texas 78284; Laboratory of Molecular Endocrinology, University of California San Francisco, California 94143

Search for other works by this author on:

,

1Department of Medicine, Division of Oncology, University of Texas Health Science Center San Antonio, Texas 78284; Laboratory of Molecular Endocrinology, University of California San Francisco, California 94143

Search for other works by this author on:

1Department of Medicine, Division of Oncology, University of Texas Health Science Center San Antonio, Texas 78284; Laboratory of Molecular Endocrinology, University of California San Francisco, California 94143

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This work was supported by NIH Grants PO1-30195 and R01-CA-30251 (to C.K.O.) and NIH Grant HD-10202 (RIA Core).

Author Notes

Revision received:

18 August 1989

Published:

01 November 1989

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C. Kent Osborne, Ester B. Coronado, Libbey J. Kitten, Carlos I. Arteaga, Suzanne A. W. Fuqua, K. Ramasharma, Milton Marshall, Choh Hao Li, Insulin-Like Growth Factor-ll (IGF-II): A Potential Autocrine/Paracrine Growth Factor for Human Breast Cancer Acting via the IGF-I Receptor, Molecular Endocrinology, Volume 3, Issue 11, 1 November 1989, Pages 1701–1709, https://doi.org/10.1210/mend-3-11-1701
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Abstract

Insulin-like growth factor-ll (IGF-II) is a potent mitogen for several types of cultured cells and tissues. We have studied the interaction of IGF-II with a panel of cultured human breast cancer cell lines, examining the possibility that these cells synthesize and secrete IGF-II activity which could have autocrine/ paracrine functions. Synthetic IGF-II was mitogenic in five of seven cell lines tested, including the estrogen receptor-positive lines MCF-7L, ZR75–1, and T47D and the estrogen receptor (ER)-negative lines Hs578T and MDA-231. IGF-II was slightly less potent than IGF-I in stimulating DNA synthesis in MCF-7I cells, an effect that paralleled its ability to compete for [125I]IGF-I binding in these cells. Affinity labeling studies revealed that IGF-II could also compete for binding to the 130,000 mol wt α-subunit of the IGF-I receptor. A monoclonal antibody to the IGF-I receptor inhibited the mitogenic effects of IGF-II in MCF-7L and MDA-231 cells, suggesting that this receptor mediates the growth effects of IGF-II in these breast cancer cells. Using a RIA and a RRA, IGF-ll-like activity was detected in conditioned medium extracts processed to remove IGF-binding proteins from several breast cancer cell lines, with the highest levels found in conditioned medium from MCF-7L and T47D cell lines. IGF-II mRNA transcripts in MCF-7L and T47D cells were identified by Northern blot analysis and were confirmed by RNase protection assay. IGF-II mRNA was increased by estrogen in MCF-7L cells. These data suggest that IGF-II is an important mitogen for certain breast cancer cells and that its effects are mediated via the IGF-I receptor. The ability of these cells to express IGF-II mRNA and secrete IGF-II activity into the culture medium further supports the hypothesis that IGF-II may have autocrine/paracrine as well as endocrine growth regulatory functions in human breast cancer.

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Author notes

This work was supported by NIH Grants PO1-30195 and R01-CA-30251 (to C.K.O.) and NIH Grant HD-10202 (RIA Core).

†

Deceased.

Copyright © 1989 by The Endocrine Society

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