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Literature summary for 2.7.1.91 extracted from

  • Dayon, A.; Brizuela, L.; Martin, C.; Mazerolles, C.; Pirot, N.; Doumerc, N.; Nogueira, L.; Golzio, M.; Teissie, J.; Serre, G.; Rischmann, P.; Malavaud, B.; Cuvillier, O.
    Sphingosine kinase-1 is central to androgen-regulated prostate cancer growth and survival (2009), PLoS ONE, 4, e8048.
    View publication on PubMedView publication on EuropePMC
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Inhibitors

Inhibitors Comment Organism Structure
additional information short-term androgen removal induces a rapid and transient SphK1 inhibition associated with a reduced cell growth in vitro and in vivo, an event that is not observed in the hormone-insensitive PC-3 cells. The addition of dihydrotestosterone to androgen-deprived LNCaP cells re-establishes cell proliferation, through an androgen receptor/PI3K/Akt dependent stimulation of SphK1, and inhibition of SphK1 can markedly impede the effects of dihydrotestosterone Homo sapiens

Organism

Organism UniProt Comment Textmining
Homo sapiens
-
-
-

Source Tissue

Source Tissue Comment Organism Textmining
LNCaP cell
-
 Homo sapiens
-
LNCAP-C4-2B cell
-
 Homo sapiens
-

Expression

Organism Comment Expression
Homo sapiens long-term removal of androgen support in LNCaP and C4-2B cells results in a progressive increase in SphK1 expression and activity throughout the progression to androgen-independence state, which is characterized by the acquisition of a neuroendocrine-like cell phenotype up

General Information

General Information Comment Organism
physiological function short-term androgen removal induces a rapid and transient SphK1 inhibition associated with a reduced cell growth in vitro and in vivo, an event that is not observed in the hormone-insensitive PC-3 cells. The addition of dihydrotestosterone to androgen-deprived LNCaP cells re-establishes cell proliferation, through an androgen receptor/PI3K/Akt dependent stimulation of SphK1, and inhibition of SphK1 can markedly impede the effects of dihydrotestosterone. Long-term removal of androgen support in LNCaP and C4-2B cells results in a progressive increase in SphK1 expression and activity throughout the progression to androgen-independence state, which is characterized by the acquisition of a neuroendocrine-like cell phenotype. Inhibition of the PI3K/Akt pathway by negatively impacting SphK1 activity can prevent neuroendocrine differentiation in both cell models, an event that can be mimicked by SphK1 inhibitors Homo sapiens