Cancer Research AACR Membership Telomeres
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
Cancer Prevention Journals Portal Cancer Reviews Online
Annual Meeting Education Book Meeting Abstracts Online
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Varma, H.
Right arrow Articles by Conrad, S. E.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Varma, H.
Right arrow Articles by Conrad, S. E.
[Cancer Research 62, 3985-3991, July 15, 2002]
© 2002 American Association for Cancer Research

Endocrinology

Antiestrogen ICI 182,780 Decreases Proliferation of Insulin-like Growth Factor I (IGF-I)-treated MCF-7 Cells without Inhibiting IGF-I Signaling1

Hemant Varma and Susan E. Conrad2

Departments of Biochemistry and Molecular Biology [H. V.] and Microbiology and Molecular Genetics [S. E. C.], Michigan State University, East Lansing, Michigan 48824

Previous studies have suggested that antiestrogens inhibit MCF-7 cell proliferation by alteringthe expression or activity of components of the insulin-like growth factor I (IGF-I) signaling pathway, including IGF-I receptor, insulin receptor substrate 1, and phosphatidylinositol 3-kinase. In this report, we examine the effects of the pure antiestrogen ICI 182,780 (ICI) on various targets of IGF-I signaling in MCF-7 cells. ICI treatment led to decreases in the absolute levels of cyclin D1 and cyclin A expression, retinoblastoma protein phosphorylation, and DNA synthesis in IGF-I-treated cells. However, IGF-I retained the ability to induce these events in the presence of ICI, suggesting that ICI treatment did not completely block IGF-I signaling. Consistent with this suggestion, IGF-I-induced phosphorylation of extracellular signal-regulated kinase, AKT, and insulin receptor substrate 1 was unaffected by ICI treatment. Finally, transient expression of either constitutively active phosphatidylinositol 3-kinase or AKT was unable to induce proliferation in ICI-treated MCF-7 cells. Together, these results indicate that ICI can inhibit proliferation without blocking IGF-I signaling and suggest a model in which both estrogen receptor and IGF-I signaling regulate cell cycle components and are required for MCF-7 cell proliferation.




This article has been cited by other articles:


Home page
 J. Biol. Chem.Home page
S. Baron, A. Escande, G. Alberola, K. Bystricky, P. Balaguer, and H. Richard-Foy
Estrogen Receptor {alpha} and the Activating Protein-1 Complex Cooperate during Insulin-like Growth Factor-I-induced Transcriptional Activation of the pS2/TFF1 Gene
J. Biol. Chem., April 20, 2007; 282(16): 11732 - 11741.
[Abstract] [Full Text] [PDF]

Home page
 Cancer Res.Home page
K. Dhar, S. Banerjee, G. Dhar, K. Sengupta, and S. K. Banerjee
Insulin-like Growth Factor-1 (IGF-1) Induces WISP-2/CCN5 via Multiple Molecular Cross-talks and Is Essential for Mitogenic Switch by IGF-1 Axis in Estrogen Receptor-Positive Breast Tumor Cells
Cancer Res., February 15, 2007; 67(4): 1520 - 1526.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
S. Cascio, V. Bartella, C. Garofalo, A. Russo, A. Giordano, and E. Surmacz
Insulin-like Growth Factor 1 Differentially Regulates Estrogen Receptor-dependent Transcription at Estrogen Response Element and AP-1 Sites in Breast Cancer Cells
J. Biol. Chem., February 9, 2007; 282(6): 3498 - 3506.
[Abstract] [Full Text] [PDF]

Home page
 J Mol EndocrinolHome page
S Zhang, X Li, R Burghardt, R Smith III, and S H Safe
Role of estrogen receptor (ER) {alpha} in insulin-like growth factor (IGF)-I-induced responses in MCF-7 breast cancer cells
J. Mol. Endocrinol., December 1, 2005; 35(3): 433 - 447.
[Abstract] [Full Text] [PDF]

Home page
 EndocrinologyHome page
J. Xu, S. Fan, and E. M. Rosen
Regulation of the Estrogen-Inducible Gene Expression Profile by the Breast Cancer Susceptibility Gene BRCA1
Endocrinology, April 1, 2005; 146(4): 2031 - 2047.
[Abstract] [Full Text] [PDF]

Home page
 J. Immunol.Home page
W. H. Shen, S. T. Jackson, S. R. Broussard, R. H. McCusker, K. Strle, G. G. Freund, R. W. Johnson, R. Dantzer, and K. W. Kelley
IL-1{beta} Suppresses Prolonged Akt Activation and Expression of E2F-1 and Cyclin A in Breast Cancer Cells
J. Immunol., June 15, 2004; 172(12): 7272 - 7281.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
W. H. Shen, Y. Yin, S. R. Broussard, R. H. McCusker, G. G. Freund, R. Dantzer, and K. W. Kelley
Tumor Necrosis Factor {alpha} Inhibits Cyclin A Expression and Retinoblastoma Hyperphosphorylation Triggered by Insulin-like Growth Factor-I Induction of New E2F-1 Synthesis
J. Biol. Chem., February 27, 2004; 279(9): 7438 - 7446.
[Abstract] [Full Text] [PDF]

Home page
 Mol. Endocrinol.Home page
E. R. Levin
Bidirectional Signaling between the Estrogen Receptor and the Epidermal Growth Factor Receptor
Mol. Endocrinol., March 1, 2003; 17(3): 309 - 317.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
Cancer Prevention Journals Portal Cancer Reviews Online
Annual Meeting Education Book Meeting Abstracts Online
Copyright © 2002 by the American Association for Cancer Research.