Sphingosine kinase-1 mediates androgen-induced osteoblast cell growth

Herein we report that the lipid kinase sphingosine kinase-1 (SphK1) is instrumental in mediating androgen-induced cell proliferation in osteoblasts. Dihydrotestosterone (DHT) triggered cell growth in steroid-deprived MC3T3 cells, which was associated with a rapid stimulation of SphK1 and activation...

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Bibliographic Details
Published in:Biochemical and biophysical research communications 2010-01, Vol.391 (1), p.669-673
Main Authors: Martin, Claire, Lafosse, Jean-Michel, Malavaud, Bernard, Cuvillier, Olivier
Format: Article
Language:English
Subjects:
60 APPLIED LIFE SCIENCES
ANDROGENS
Androgens - metabolism
Androgens - pharmacology
ANIMAL GROWTH
Animals
Cell Line
CELL PROLIFERATION
CHARCOAL
CONNECTIVE TISSUE CELLS
Dihydrotestosterone - metabolism
Dihydrotestosterone - pharmacology
ERK1/2
INHIBITION
LIPIDS
Mice
Osteoblasts
Osteoblasts - drug effects
Osteoblasts - enzymology
Osteoblasts - physiology
Phosphatidylinositol 3-Kinases - metabolism
Phosphotransferases (Alcohol Group Acceptor) - antagonists & inhibitors
Phosphotransferases (Alcohol Group Acceptor) - metabolism
PI3K
Proto-Oncogene Proteins c-akt - metabolism
RECEPTORS
Receptors, Androgen - metabolism
SIGNALS
Sphingosine kinase-1
STIMULATION
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Summary:Herein we report that the lipid kinase sphingosine kinase-1 (SphK1) is instrumental in mediating androgen-induced cell proliferation in osteoblasts. Dihydrotestosterone (DHT) triggered cell growth in steroid-deprived MC3T3 cells, which was associated with a rapid stimulation of SphK1 and activation of both Akt and ERK signaling pathways. This mechanism relied on functional androgen receptor/PI3K/Akt nongenotropic signaling as pharmacological antagonists could block SphK1 stimulation by DHT and its consequences. Finally, SphK1 inhibition not only abrogated DHT-induced ERK activation but also blocked cell proliferation, while ERK inhibition had no impact, suggesting that SphK1 was critical for DHT signaling yet independently of the ERK.
ISSN:0006-291X
1090-2104
DOI:10.1016/j.bbrc.2009.11.118