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S1P2 receptors mediate inhibition of glioma cell migration through Rho signaling pathways independent of PTEN
- Source :
- Biochemical and Biophysical Research Communications. 366:963-968
- Publication Year :
- 2008
- Publisher :
- Elsevier BV, 2008.
-
Abstract
- Sphingosine 1-phosphate (S1P) induced the inhibition of glioma cell migration. Here, we characterized the signaling mechanisms involved in the inhibitory action by S1P. In human GNS-3314 glioblastoma cells, the S1P-induced inhibition of cell migration was associated with activation of RhoA and suppression of Rac1. The inhibitory action of S1P was recovered by a small interference RNA specific to S1P(2) receptor, a carboxyl-terminal region of Galpha12 or Galpha13, an RGS domain of p115RhoGEF, and a dominant-negative mutant of RhoA. The inhibitory action of S1P through S1P(2) receptors was also observed in both U87MG glioblastoma and 1321N1 astrocytoma cells, which have no protein expression of a phosphatase and tensin homolog deleted on chromosome 10 (PTEN). These results suggest that S1P(2) receptors/G(12/13)-proteins/Rho signaling pathways mediate S1P-induced inhibition of glioma cell migration. However, PTEN, recently postulated as an indispensable molecule for the inhibition of cell migration, may not be critical for the S1P(2) receptor-mediated action in glioma cells.
- Subjects :
- rac1 GTP-Binding Protein
RHOA
Biophysics
RAC1
GTP-Binding Protein alpha Subunits, G12-G13
Biochemistry
chemistry.chemical_compound
Cell Movement
Sphingosine
Cell Line, Tumor
Glioma
medicine
Humans
PTEN
Tensin
Receptor
Molecular Biology
biology
organic chemicals
PTEN Phosphohydrolase
Cell migration
Cell Biology
medicine.disease
Cell biology
Receptors, Lysosphingolipid
chemistry
biology.protein
Cancer research
lipids (amino acids, peptides, and proteins)
Lysophospholipids
rhoA GTP-Binding Protein
Signal Transduction
Subjects
Details
- ISSN :
- 0006291X
- Volume :
- 366
- Database :
- OpenAIRE
- Journal :
- Biochemical and Biophysical Research Communications
- Accession number :
- edsair.doi.dedup.....c04fd5cb7b63185fa59eaa1eb112d48b