Androgen Induction of Follicular Epithelial Cell Growth Is Mediated via Insulin-like Growth Factor-I from Dermal Papilla Cells

1995 ◽  
Vol 212 (3) ◽  
pp. 988-994 ◽  
Author(s):  
S. Itami ◽  
S. Kurata ◽  
S. Takayasu
Keyword(s):  
Growth Factor ◽  
Cell Growth ◽  
Epithelial Cell ◽  
Dermal Papilla ◽  
Insulin Like Growth Factor ◽  
Dermal Papilla Cells ◽  
Factor I ◽  
Follicular Epithelial Cell ◽  
Growth Factor I ◽  
Follicular Epithelial

scholarly journals Serine Phosphorylation of the Insulin-like Growth Factor I (IGF-1) Receptor C-terminal Tail Restrains Kinase Activity and Cell Growth

2012 ◽  
Vol 287 (33) ◽  
pp. 28180-28194 ◽  
Author(s):  
Geraldine M. Kelly ◽  
Deirdre A. Buckley ◽  
Patrick A. Kiely ◽  
David R. Adams ◽  
Rosemary O'Connor
Keyword(s):  
Growth Factor ◽  
Cell Growth ◽  
Kinase Activity ◽  
Serine Phosphorylation ◽  
Insulin Like Growth Factor ◽  
Factor I ◽  
Growth Factor I

Insulin-like growth factor I is a dual effector of multiple myeloma cell growth

Blood ◽  
2000 ◽  
Vol 96 (8) ◽  
pp. 2856-2861 ◽  
Author(s):  
Nie-Lin Ge ◽  
Stuart Rudikoff
Keyword(s):  
Multiple Myeloma ◽  
Growth Factor ◽  
Cell Growth ◽  
Myeloma Cell ◽  
Mitogen Activated Protein Kinase ◽  
Insulin Like Growth Factor ◽  
Factor I ◽  
Igf I ◽  
Growth Factor I

Abstract Multiple myeloma (MM) is an invariably fatal disease that accounts for approximately 1% to 2% of all human cancers. Surprisingly little is known about the cellular pathways contributing to growth of these tumors. Although the cytokine interleukin-6 has been suggested to be the major stimulus for myeloma cell growth, the role of a second potential growth factor, insulin-like growth factor I (IGF-I), has been less clearly defined. The IGF-I signaling cascade in 8 MM cell lines was examined. In 7 of these, the IGF-I receptor (IGF-IR) was expressed and autophosphorylated in response to ligand. Downstream of IGF-IR, insulin receptor substrate 1 was phosphorylated, leading to the activation of phosphatidylinositol-3′-kinase (PI-3K). PI-3K, in turn, regulated 2 distinct pathways. The first included Akt and Bad, leading to an inhibition of apoptosis; the second included the mitogen-activated protein kinase (MAPK), resulting in proliferation. Biologic relevance of this pathway was demonstrated because in vitro IGF-I induced both an antiapoptotic and a proliferative effect. Importantly, in vivo administration of IGF-I in SCID mice inoculated with the OPM-2 line led to approximately twice the growth rate of tumor cells as in controls. These results suggest that IGF-I activates at least 2 pathways effecting myeloma cell growth and contributes significantly to expansion of these cells in vivo.

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