| Literature DB >> 24486401 |
Jan Ohotski1, Hugh Rosen2, Robert Bittman3, Susan Pyne1, Nigel J Pyne4.
Abstract
We demonstrate that pre-treatment of estrogen receptor negative MDA-MB-231 breast cancer cells containing ectopically expressed HA-tagged sphingosine 1-phosphate receptor-2 (S1P2) with the sphingosine kinase 1/2 inhibitor SKi (2-(p-hydroxyanilino)-4-(p-chlorophenyl)thiazole) or the sphingosine kinase 2 selective inhibitor (R)-FTY720 methyl ether (ROMe) or sphingosine kinase 2 siRNA induced the translocation of HA-tagged S1P2 and Y416 phosphorylated c-Src to the nucleus of these cells. This is associated with reduced growth of HA-tagged S1P2 over-expressing MDA-MB-231 cells. Treatment of HA-S1P2 over-expressing MDA-MB-231 cells with the sphingosine 1-phosphate receptor-4 (S1P4) antagonist CYM50367 or with S1P4 siRNA also promoted nuclear translocation of HA-tagged S1P2. These findings identify for the first time a signaling pathway in which sphingosine 1-phosphate formed by sphingosine kinase 2 binds to S1P4 to prevent nuclear translocation of S1P2 and thereby promote the growth of estrogen receptor negative breast cancer cells.Entities:
Keywords: Cancer; Growth; Nuclear signaling; Sphingosine 1-phosphate; Sphingosine 1-phosphate receptors; Sphingosine kinase
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Year: 2014 PMID: 24486401 DOI: 10.1016/j.cellsig.2014.01.023
Source DB: PubMed Journal: Cell Signal ISSN: 0898-6568 Impact factor: 4.315