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• W2040480415 abstract "Abstract Sphingosine‐1‐phosphate (S1P) is a bioactive lipid that signals through a family of G protein‐coupled receptors consisting of 5 members termed S1P 1–5 , and it regulates cellular proliferation, migration and survival. We investigated the expression and role of S1P receptors in glioma. Human glioma expressed S1P 1 , S1P 2 , S1P 3 , and S1P 5 by quantitative real‐time PCR analysis. Expression of the S1P 1 was significantly lower in glioblastoma than in the normal brain ( p < 0.01) and diffuse astrocytoma ( p < 0.05). Immunoblotting showed that normal brain expressed more S1P 1 protein than did glioblastoma. Immunohistochemistry showed that S1P 1 was localized predominantly in the astrocytes in the normal brain, but no staining was observed in glioblastoma. Downregulation of S1P 1 expression correlated with poor survival of patients with glioblastoma ( p < 0.05). S1P 1 small interfering RNA promoted cell proliferation in high‐expressor glioma cell lines (T98G, G112). Cell proliferation was promoted by the pertussis toxin, which deactivates G i/o type of G proteins; the S1P 1 is exclusively coupled to these proteins. Forced expression of the S1P 1 in low‐expressor cell lines (U87, U251) resulted in decreased cell growth and led to suppressed tumor growth in transplanted gliomas in vivo . Furthermore, we found a significant association between the S1P 1 expression and early growth response‐1, a transcriptional factor that exhibits tumor suppression in glioblastoma cells ( p < 0.05). These data indicate that the downregulation of S1P 1 expression enhances the malignancy of glioblastoma by increasing cell proliferation and correlates with the shorter survival of patients with glioblastoma." @default.
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• W2040480415 date "2010-01-08" @default.
• W2040480415 modified "2023-10-18" @default.
• W2040480415 title "Sphingosine-1-phosphate receptor type 1 regulates glioma cell proliferation and correlates with patient survival" @default.
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• W2040480415 doi "https://doi.org/10.1002/ijc.24933" @default.
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