|
|
 Previous Article | Table of Contents | Next Article 
Growth-promoting effects of insulin-like growth factor-1 (IGF-1) on
hematopoietic cells: overexpression of introduced IGF-1 receptor abrogates
interleukin-3 dependency of murine factor-dependent cells by a
ligand-dependent mechanism
JA McCubrey, LS Steelman, MW Mayo, PA Algate, RA Dellow and M Kaleko
Department of Microbiology and Immunology, East Carolina University School
of Medicine, Greenville, NC 27858.
Although insulin-like growth factor (IGF-1) stimulated 3H-thymidine
incorporation upon addition to the interleukin-3 (IL-3)-dependent cell line
FDC-P1, IGF-1 did not relieve IL-3 dependency for growth. To further
examine the effects of IGF-1 on hematopoietic cells, FDC-P1 cells were
infected with a retroviral construct (LISN) containing the human IGF-1
receptor (hIGF-1R) and neo genes. IL-3-independent cells were readily
isolated after LISN infection when either IGF-1 or supraphysiologic
concentrations of insulin were included in the culture medium. These cells
were transformed to IL-3 independence by a ligand- dependent mechanism
because their growth was dependent on the presence of either IGF-1 or
insulin and growth factors capable of supporting autocrine growth were not
detected. Furthermore, a monoclonal antibody (MoAb) directed against the
human IGF-1R (alpha IR-3) inhibited IGF-1 but not IL-3-induced
proliferation and these cells contained 20- to 200- fold more IGF-1
receptors than uninfected FDC-P1 cells. In contrast, when LISN-infected
cells were plated in medium without exogenously supplied IGF-1 or insulin,
factor-independent cells were rarely isolated. Growth of these cells was
also inhibited by the alpha IR-3 MoAb and they expressed 100- to 400-fold
more IGF-1 receptors than uninfected FDC-P1 cells. The endogenous IGF-1
and/or insulin present in the calf serum may have enabled their growth
because these cells, unlike the parental cells, would proliferate in
serum-free defined media and their growth was again inhibited by the alpha
IR-3 MoAb. These results demonstrate that IGF-1 can replace IL-3 for growth
when FDC-P1 cells overexpress the IGF-1R. Given the fairly ubiquitous
expression of the IGF-1 receptor, these and additional experiments might
help to determine whether increased expression of endogenous receptors by
cells can lead to leukemogenesis and tumorigenesis. Moreover,
hIGF-1R-infected cells will be useful in investigating the mechanisms of
IGF1-mediated signal transduction because they are now known to proliferate
in response to IGF-1.
Volume 78,
Issue 4,
pp. 921-929,
08/15/1991
Copyright © 1991 by The American Society of Hematology
 CiteULike  Connotea  Del.icio.us  Digg  Reddit  Technorati What's this?
This article has been cited by other articles:
|
|
|
|
 
Y.-W. Chu, S. Schmitz, B. Choudhury, W. Telford, V. Kapoor, S. Garfield, D. Howe, and R. E. Gress
Exogenous insulin-like growth factor 1 enhances thymopoiesis predominantly through thymic epithelial cell expansion
Blood,
October 1, 2008;
112(7):
2836 - 2846.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
Y. Toyoshima, M. Karas, S. Yakar, J. Dupont, Lee Helman, and D. LeRoith
TDAG51 Mediates the Effects of Insulin-like Growth Factor I (IGF-I) on Cell Survival
J. Biol. Chem.,
June 11, 2004;
279(24):
25898 - 25904.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. Sekharam, H. Zhao, M. Sun, Q. Fang, Q. Zhang, Z. Yuan, H. C. Dan, D. Boulware, J. Q. Cheng, and D. Coppola
Insulin-like Growth Factor 1 Receptor Enhances Invasion and Induces Resistance to Apoptosis of Colon Cancer Cells through the Akt/Bcl-xL Pathway
Cancer Res.,
November 15, 2003;
63(22):
7708 - 7716.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
A. Hongo, H. Kuramoto, Y. Nakamura, K. Hasegawa, K. Nakamura, J. Kodama, and Y. Hiramatsu
Antitumor Effects of a Soluble Insulin-Like Growth Factor I Receptor in Human Ovarian Cancer Cells: Advantage of Recombinant Protein Administration in Vivo
Cancer Res.,
November 15, 2003;
63(22):
7834 - 7839.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. R. DiFalco, S. Ali, and L. F. Congote
The improved survival of hematopoietic cells cultured with a fusion protein of insulin-like growth factor II (IGF-II) and interleukin 3 (IL-3) is associated with increases in Bcl-xL and phosphatidylinositol-3 kinase activity
J. Leukoc. Biol.,
February 1, 2003;
73(2):
297 - 305.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
C. S. Carter, M. M. Ramsey, R. L. Ingram, A. B. Cashion, W. T. Cefalu, Z.Q. Wang, and W. E. Sonntag
Models of Growth Hormone and IGF-1 Deficiency: Applications to Studies of Aging Processes and Life-Span Determination
J. Gerontol. A Biol. Sci. Med. Sci.,
May 1, 2002;
57(5):
B177 - 188.
[Abstract]
[Full Text]
|
|
|
|
|
|
|
M. Navarro and R. Baserga
Limited Redundancy of Survival Signals from the Type 1 Insulin-Like Growth Factor Receptor
Endocrinology,
March 1, 2001;
142(3):
1073 - 1081.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
F. Peruzzi, M. Prisco, M. Dews, P. Salomoni, E. Grassilli, G. Romano, B. Calabretta, and R. Baserga
Multiple Signaling Pathways of the Insulin-Like Growth Factor 1 Receptor in Protection from Apoptosis
Mol. Cell. Biol.,
October 1, 1999;
19(10):
7203 - 7215.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
B. Valentinis, G. Romano, F. Peruzzi, A. Morrione, M. Prisco, S. Soddu, B. Cristofanelli, A. Sacchi, and R. Baserga
Growth and Differentiation Signals by the Insulin-like Growth Factor 1 Receptor in Hemopoietic Cells Are Mediated through Different Pathways
J. Biol. Chem.,
April 30, 1999;
274(18):
12423 - 12430.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
C. Ohlsson, N. Kley, H. Werner, and D. LeRoith
p53 Regulates Insulin-Like Growth Factor-I (IGF-I) Receptor Expression and IGF-I-Induced Tyrosine Phosphorylation in an Osteosarcoma Cell Line: Interaction between p53 and Sp1
Endocrinology,
March 1, 1998;
139(3):
1101 - 1107.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
S. Li, M. Resnicoff, and R. Baserga
Effect of Mutations at Serines 1280-1283 on the Mitogenic and Transforming Activities of the Insulin-like Growth Factor I Receptor
J. Biol. Chem.,
May 24, 1996;
271(21):
12254 - 12260.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. Miura, E. Surmacz, J.-L. Burgaud, and R. Baserga
Different Effects on Mitogenesis and Transformation of a Mutation at Tyrosine 1251 of the Insulin-like Growth Factor I Receptor
J. Biol. Chem.,
September 22, 1995;
270(38):
22639 - 22644.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
J. Du and P. Delafontaine
Inhibition of Vascular Smooth Muscle Cell Growth Through Antisense Transcription of a Rat Insulin-Like Growth Factor I Receptor cDNA
Circ. Res.,
June 1, 1995;
76(6):
963 - 972.
[Abstract]
[Full Text]
|
|
|
|
|
|
|
L. Wang, M. Myers Jr, X. Sun, S. Aaronson, M White, and J. Pierce
IRS-1: essential for insulin- and IL-4-stimulated mitogenesis in hematopoietic cells
Science,
September 17, 1993;
261(5128):
1591 - 1594.
[Abstract]
[PDF]
|
|
|
|
|
|
|
B. Valentinis, M. Navarro, T. Zanocco-Marani, P. Edmonds, J. McCormick, A. Morrione, A. Sacchi, G. Romano, K. Reiss, and R. Baserga
Insulin Receptor Substrate-1, p70S6K, and Cell Size in Transformation and Differentiation of Hemopoietic Cells
J. Biol. Chem.,
August 11, 2000;
275(33):
25451 - 25459.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
A.-M. Khatib, G. Siegfried, A. Prat, J. Luis, M. Chretien, P. Metrakos, and N. G. Seidah
Inhibition of Proprotein Convertases Is Associated with Loss of Growth and Tumorigenicity of HT-29 Human Colon Carcinoma Cells. IMPORTANCE OF INSULIN-LIKE GROWTH FACTOR-1 (IGF-1) RECEPTOR PROCESSING IN IGF-1-MEDIATED FUNCTIONS
J. Biol. Chem.,
August 10, 2001;
276(33):
30686 - 30693.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
J. Dupont, A. M. Fernandez, C. A. Glackin, L. Helman, and D. LeRoith
Insulin-like Growth Factor 1 (IGF-1)-induced Twist Expression Is Involved in the Anti-apoptotic Effects of the IGF-1 Receptor
J. Biol. Chem.,
July 6, 2001;
276(28):
26699 - 26707.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
