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000212428 1001_ $$0P:(DE-He78)1875dd3a72033b3b8b5b55d10c6229dd$$aArseni, Lavinia$$b0$$eFirst author$$udkfz
000212428 245__ $$aSphingosine-1-Phosphate Recruits Macrophages and Microglia and Induces a Pro-Tumorigenic Phenotype That Favors Glioma Progression.
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000212428 520__ $$aGlioblastoma is the most aggressive brain tumor in adults. Treatment failure is predominantly caused by its high invasiveness and its ability to induce a supportive microenvironment. As part of this, a major role for tumor-associated macrophages/microglia (TAMs) in glioblastoma development was recognized. Phospholipids are important players in various fundamental biological processes, including tumor-stroma crosstalk, and the bioactive lipid sphingosine-1-phosphate (S1P) has been linked to glioblastoma cell proliferation, invasion, and survival. Despite the urgent need for better therapeutic approaches, novel strategies targeting sphingolipids in glioblastoma are still poorly explored. Here, we showed that higher amounts of S1P secreted by glioma cells are responsible for an active recruitment of TAMs, mediated by S1P receptor (S1PR) signaling through the modulation of Rac1/RhoA. This resulted in increased infiltration of TAMs in the tumor, which, in turn, triggered their pro-tumorigenic phenotype through the inhibition of NFkB-mediated inflammation. Gene set enrichment analyses showed that such an anti-inflammatory microenvironment correlated with shorter survival of glioblastoma patients. Inhibition of S1P restored a pro-inflammatory phenotype in TAMs and resulted in increased survival of tumor-bearing mice. Taken together, our results establish a crucial role for S1P in fine-tuning the crosstalk between glioma and infiltrating TAMs, thus pointing to the S1P-S1PR axis as an attractive target for glioma treatment.
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000212428 650_7 $$2Other$$aS1P
000212428 650_7 $$2Other$$aanti-inflammatory
000212428 650_7 $$2Other$$aglioblastoma
000212428 650_7 $$2Other$$amicroenvironment
000212428 650_7 $$2Other$$atumor-associated macrophages/microglia
000212428 7001_ $$0P:(DE-He78)712670f67b229b25980c0e1c88ae8a09$$aSharma, Rakesh$$b1
000212428 7001_ $$0P:(DE-He78)e73a0a4fab40344d89d693cbe1df3109$$aMack, Norman$$b2$$udkfz
000212428 7001_ $$0P:(DE-He78)22d5965a3a728414a0fd8c37639a1e99$$aNagalla, Deepthi$$b3
000212428 7001_ $$0P:(DE-He78)5ad7de84a84805746cf4d7f7f90cdbff$$aOhl, Sibylle$$b4$$udkfz
000212428 7001_ $$0P:(DE-He78)743a4a82daab55306a2c88b9f6bf8c2f$$aHielscher, Thomas$$b5$$udkfz
000212428 7001_ $$0P:(DE-He78)1956b17ee4a34a5fdd72287aca7cdc0a$$aSinghal, Mahak$$b6$$udkfz
000212428 7001_ $$0P:(DE-He78)b311cdc556fc52393ea4902245ec422b$$aEngel, Robert$$b7$$udkfz
000212428 7001_ $$0P:(DE-He78)2e92d0ae281932fc7347d819fec36b0b$$aAugustin, Hellmut$$b8$$udkfz
000212428 7001_ $$0P:(DE-He78)a928ded2085c8911822370cad0b4a728$$aSandhoff, Roger$$b9$$udkfz
000212428 7001_ $$aHerold-Mende, Christel$$b10
000212428 7001_ $$0P:(DE-He78)a33ae52a1d80b847405db3ab83b9e90d$$aTews, Björn$$b11
000212428 7001_ $$0P:(DE-He78)e13b4363c5fe858044ef8a39c02c870c$$aLichter, Peter$$b12$$udkfz
000212428 7001_ $$0P:(DE-He78)e67f907703fcb2cf909f4d72d50268b5$$aSeiffert, Martina$$b13$$eLast author$$udkfz
000212428 773__ $$0PERI:(DE-600)2527080-1$$a10.3390/cancers15020479$$gVol. 15, no. 2, p. 479 -$$n2$$p479$$tCancers$$v15$$x2072-6694$$y2023
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