Multihormonal regulation of insulin-like growth factor-I-related protein in MCF-7 human breast cancer cells

K. K. Huff, C. Knabbe, R. Lindsey, D. Kaufman, D. Bronzert, Marc E Lippman, R. B. Dickson

Research output: Contribution to journalArticle

124 Citations (Scopus)

Abstract

MCF-7 human breast cancer cells have been studied for hormonal regulation of secretion of an insulin growth factor-I (IGF-I)-related growth factor. 17β-Estradiol, which is required for tumorigenesis of the cell line in the nude mouse and which stimulates proliferation in vitro, was able to significantly induce IGF-I secretion at 10-13 M, with maximal induction at 10-11 M. Under optimal conditions IGF-I could be induced 4-fold after 4 days. Demonstration of estrogenic stimulations required removal of phenol red, a weak estrogen, from the cell culture medium. In addition to estrogen, insulin, epidermal growth factor, and transforming growth factor α induce both cellular proliferation and IGF-I secretion, while growth inhibitory antiestrogens, transforming growth factor β, and glucocorticoids have the opposite effect. In each case, modulations in IGF-I secretion preceeded effects on cellular proliferation. IGF-I was not regulated by human GH, basic fibroblast growth factor, platelet-derived growth factor, or PRL, none of which affected proliferation rate. Thus, regulation of IGF-I secretion in human breast cancer is controlled by different hormones from those previously reported in human fibroblasts. Regulation of IGF-I by neither estrogen nor antiestrogen was associated with changes in steady-state mRNA levels; thus regulation may occur at a step beyond mRNA. We conclude that IGF-I production is tightly coupled to growth regulation by estrogens, antiestrogens, and other hormones and may contribute to autocrine and/or paracrine growth regulation by these agents in breast cancer.

Original languageEnglish
Pages (from-to)200-208
Number of pages9
JournalMolecular Endocrinology
Volume2
Issue number3
StatePublished - Jan 1 1988
Externally publishedYes

Fingerprint

Insulin-Like Growth Factor I
Intercellular Signaling Peptides and Proteins
Insulin
Breast Neoplasms
Proteins
Estrogen Receptor Modulators
Estrogens
Transforming Growth Factors
Growth
Cell Proliferation
Hormones
Phenolsulfonphthalein
Messenger RNA
Platelet-Derived Growth Factor
Fibroblast Growth Factor 2
Epidermal Growth Factor
Nude Mice
Glucocorticoids
Culture Media
Estradiol

ASJC Scopus subject areas

  • Molecular Biology
  • Endocrinology, Diabetes and Metabolism

Cite this

Huff, K. K., Knabbe, C., Lindsey, R., Kaufman, D., Bronzert, D., Lippman, M. E., & Dickson, R. B. (1988). Multihormonal regulation of insulin-like growth factor-I-related protein in MCF-7 human breast cancer cells. Molecular Endocrinology, 2(3), 200-208.

Multihormonal regulation of insulin-like growth factor-I-related protein in MCF-7 human breast cancer cells. / Huff, K. K.; Knabbe, C.; Lindsey, R.; Kaufman, D.; Bronzert, D.; Lippman, Marc E; Dickson, R. B.

In: Molecular Endocrinology, Vol. 2, No. 3, 01.01.1988, p. 200-208.

Research output: Contribution to journalArticle

Huff, KK, Knabbe, C, Lindsey, R, Kaufman, D, Bronzert, D, Lippman, ME & Dickson, RB 1988, 'Multihormonal regulation of insulin-like growth factor-I-related protein in MCF-7 human breast cancer cells', Molecular Endocrinology, vol. 2, no. 3, pp. 200-208.
Huff KK, Knabbe C, Lindsey R, Kaufman D, Bronzert D, Lippman ME et al. Multihormonal regulation of insulin-like growth factor-I-related protein in MCF-7 human breast cancer cells. Molecular Endocrinology. 1988 Jan 1;2(3):200-208.
Huff, K. K. ; Knabbe, C. ; Lindsey, R. ; Kaufman, D. ; Bronzert, D. ; Lippman, Marc E ; Dickson, R. B. / Multihormonal regulation of insulin-like growth factor-I-related protein in MCF-7 human breast cancer cells. In: Molecular Endocrinology. 1988 ; Vol. 2, No. 3. pp. 200-208.
@article{5570d846b0274d80957fe77675b768df,
title = "Multihormonal regulation of insulin-like growth factor-I-related protein in MCF-7 human breast cancer cells",
abstract = "MCF-7 human breast cancer cells have been studied for hormonal regulation of secretion of an insulin growth factor-I (IGF-I)-related growth factor. 17β-Estradiol, which is required for tumorigenesis of the cell line in the nude mouse and which stimulates proliferation in vitro, was able to significantly induce IGF-I secretion at 10-13 M, with maximal induction at 10-11 M. Under optimal conditions IGF-I could be induced 4-fold after 4 days. Demonstration of estrogenic stimulations required removal of phenol red, a weak estrogen, from the cell culture medium. In addition to estrogen, insulin, epidermal growth factor, and transforming growth factor α induce both cellular proliferation and IGF-I secretion, while growth inhibitory antiestrogens, transforming growth factor β, and glucocorticoids have the opposite effect. In each case, modulations in IGF-I secretion preceeded effects on cellular proliferation. IGF-I was not regulated by human GH, basic fibroblast growth factor, platelet-derived growth factor, or PRL, none of which affected proliferation rate. Thus, regulation of IGF-I secretion in human breast cancer is controlled by different hormones from those previously reported in human fibroblasts. Regulation of IGF-I by neither estrogen nor antiestrogen was associated with changes in steady-state mRNA levels; thus regulation may occur at a step beyond mRNA. We conclude that IGF-I production is tightly coupled to growth regulation by estrogens, antiestrogens, and other hormones and may contribute to autocrine and/or paracrine growth regulation by these agents in breast cancer.",
author = "Huff, {K. K.} and C. Knabbe and R. Lindsey and D. Kaufman and D. Bronzert and Lippman, {Marc E} and Dickson, {R. B.}",
year = "1988",
month = "1",
day = "1",
language = "English",
volume = "2",
pages = "200--208",
journal = "Molecular Endocrinology",
issn = "0888-8809",
publisher = "The Endocrine Society",
number = "3",

}

TY - JOUR

T1 - Multihormonal regulation of insulin-like growth factor-I-related protein in MCF-7 human breast cancer cells

AU - Huff, K. K.

AU - Knabbe, C.

AU - Lindsey, R.

AU - Kaufman, D.

AU - Bronzert, D.

AU - Lippman, Marc E

AU - Dickson, R. B.

PY - 1988/1/1

Y1 - 1988/1/1

N2 - MCF-7 human breast cancer cells have been studied for hormonal regulation of secretion of an insulin growth factor-I (IGF-I)-related growth factor. 17β-Estradiol, which is required for tumorigenesis of the cell line in the nude mouse and which stimulates proliferation in vitro, was able to significantly induce IGF-I secretion at 10-13 M, with maximal induction at 10-11 M. Under optimal conditions IGF-I could be induced 4-fold after 4 days. Demonstration of estrogenic stimulations required removal of phenol red, a weak estrogen, from the cell culture medium. In addition to estrogen, insulin, epidermal growth factor, and transforming growth factor α induce both cellular proliferation and IGF-I secretion, while growth inhibitory antiestrogens, transforming growth factor β, and glucocorticoids have the opposite effect. In each case, modulations in IGF-I secretion preceeded effects on cellular proliferation. IGF-I was not regulated by human GH, basic fibroblast growth factor, platelet-derived growth factor, or PRL, none of which affected proliferation rate. Thus, regulation of IGF-I secretion in human breast cancer is controlled by different hormones from those previously reported in human fibroblasts. Regulation of IGF-I by neither estrogen nor antiestrogen was associated with changes in steady-state mRNA levels; thus regulation may occur at a step beyond mRNA. We conclude that IGF-I production is tightly coupled to growth regulation by estrogens, antiestrogens, and other hormones and may contribute to autocrine and/or paracrine growth regulation by these agents in breast cancer.

AB - MCF-7 human breast cancer cells have been studied for hormonal regulation of secretion of an insulin growth factor-I (IGF-I)-related growth factor. 17β-Estradiol, which is required for tumorigenesis of the cell line in the nude mouse and which stimulates proliferation in vitro, was able to significantly induce IGF-I secretion at 10-13 M, with maximal induction at 10-11 M. Under optimal conditions IGF-I could be induced 4-fold after 4 days. Demonstration of estrogenic stimulations required removal of phenol red, a weak estrogen, from the cell culture medium. In addition to estrogen, insulin, epidermal growth factor, and transforming growth factor α induce both cellular proliferation and IGF-I secretion, while growth inhibitory antiestrogens, transforming growth factor β, and glucocorticoids have the opposite effect. In each case, modulations in IGF-I secretion preceeded effects on cellular proliferation. IGF-I was not regulated by human GH, basic fibroblast growth factor, platelet-derived growth factor, or PRL, none of which affected proliferation rate. Thus, regulation of IGF-I secretion in human breast cancer is controlled by different hormones from those previously reported in human fibroblasts. Regulation of IGF-I by neither estrogen nor antiestrogen was associated with changes in steady-state mRNA levels; thus regulation may occur at a step beyond mRNA. We conclude that IGF-I production is tightly coupled to growth regulation by estrogens, antiestrogens, and other hormones and may contribute to autocrine and/or paracrine growth regulation by these agents in breast cancer.

UR - http://www.scopus.com/inward/record.url?scp=0023883779&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0023883779&partnerID=8YFLogxK

M3 - Article

VL - 2

SP - 200

EP - 208

JO - Molecular Endocrinology

JF - Molecular Endocrinology

SN - 0888-8809

IS - 3

ER -