The Putative S1PR1 Modulator ACT-209905 Impairs Growth and Migration of Glioblastoma Cells In Vitro
Glioblastoma (GBM) is still a deadly tumor due to its highly infiltrative growth behavior and its resistance to therapy. Evidence is accumulating that sphingosine-1-phosphate (S1P) acts as an important tumor-promoting molecule that is involved in the activation of the S1P receptor subtype 1 (S1PR1)....
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| Veröffentlicht in: | Cancers 2023-08, Vol.15 (17), p.4273 |
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| creator | Bien-Möller, Sandra Chen, Fan Xiao, Yong Köppe, Hanjo Jedlitschky, Gabriele Meyer, Ulrike Tolksdorf, Céline Grube, Markus Marx, Sascha Tzvetkov, Mladen V Schroeder, Henry W. S Rauch, Bernhard H |
| description | Glioblastoma (GBM) is still a deadly tumor due to its highly infiltrative growth behavior and its resistance to therapy. Evidence is accumulating that sphingosine-1-phosphate (S1P) acts as an important tumor-promoting molecule that is involved in the activation of the S1P receptor subtype 1 (S1PR1). Therefore, we investigated the effect of ACT-209905 (a putative S1PR1 modulator) on the growth of human (primary cells, LN-18) and murine (GL261) GBM cells. The viability and migration of GBM cells were both reduced by ACT-209905. Furthermore, co-culture with monocytic THP-1 cells or conditioned medium enhanced the viability and migration of GBM cells, suggesting that THP-1 cells secrete factors which stimulate GBM cell growth. ACT-209905 inhibited the THP-1-induced enhancement of GBM cell growth and migration. Immunoblot analyses showed that ACT-209905 reduced the activation of growth-promoting kinases (p38, AKT1 and ERK1/2), whereas THP-1 cells and conditioned medium caused an activation of these kinases. In addition, ACT-209905 diminished the surface expression of pro-migratory molecules and reduced CD62P-positive GBM cells. In contrast, THP-1 cells increased the ICAM-1 and P-Selectin content of GBM cells which was reversed by ACT-209905. In conclusion, our study suggests the role of S1PR1 signaling in the growth of GBM cells and gives a partial explanation for the pro-tumorigenic effects that macrophages might have on GBM cells. |
| doi_str_mv | 10.3390/cancers15174273 |
| format | Article |
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S ; Rauch, Bernhard H</creator><creatorcontrib>Bien-Möller, Sandra ; Chen, Fan ; Xiao, Yong ; Köppe, Hanjo ; Jedlitschky, Gabriele ; Meyer, Ulrike ; Tolksdorf, Céline ; Grube, Markus ; Marx, Sascha ; Tzvetkov, Mladen V ; Schroeder, Henry W. S ; Rauch, Bernhard H</creatorcontrib><description>Glioblastoma (GBM) is still a deadly tumor due to its highly infiltrative growth behavior and its resistance to therapy. Evidence is accumulating that sphingosine-1-phosphate (S1P) acts as an important tumor-promoting molecule that is involved in the activation of the S1P receptor subtype 1 (S1PR1). Therefore, we investigated the effect of ACT-209905 (a putative S1PR1 modulator) on the growth of human (primary cells, LN-18) and murine (GL261) GBM cells. The viability and migration of GBM cells were both reduced by ACT-209905. Furthermore, co-culture with monocytic THP-1 cells or conditioned medium enhanced the viability and migration of GBM cells, suggesting that THP-1 cells secrete factors which stimulate GBM cell growth. ACT-209905 inhibited the THP-1-induced enhancement of GBM cell growth and migration. Immunoblot analyses showed that ACT-209905 reduced the activation of growth-promoting kinases (p38, AKT1 and ERK1/2), whereas THP-1 cells and conditioned medium caused an activation of these kinases. In addition, ACT-209905 diminished the surface expression of pro-migratory molecules and reduced CD62P-positive GBM cells. In contrast, THP-1 cells increased the ICAM-1 and P-Selectin content of GBM cells which was reversed by ACT-209905. In conclusion, our study suggests the role of S1PR1 signaling in the growth of GBM cells and gives a partial explanation for the pro-tumorigenic effects that macrophages might have on GBM cells.</description><identifier>ISSN: 2072-6694</identifier><identifier>EISSN: 2072-6694</identifier><identifier>DOI: 10.3390/cancers15174273</identifier><identifier>PMID: 37686550</identifier><language>eng</language><publisher>Basel: MDPI AG</publisher><subject>AKT1 protein ; Amino acids ; Cancer ; Cell culture ; Cell growth ; Extracellular signal-regulated kinase ; Glioblastoma ; Glioblastoma cells ; Glioblastoma multiforme ; Intercellular adhesion molecule 1 ; Kinases ; Leukocyte migration ; Macrophages ; Medical prognosis ; Monocytes ; Motility ; P-selectin ; Sphingosine ; Sphingosine 1-phosphate ; Tumors</subject><ispartof>Cancers, 2023-08, Vol.15 (17), p.4273</ispartof><rights>COPYRIGHT 2023 MDPI AG</rights><rights>2023 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). 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ACT-209905 inhibited the THP-1-induced enhancement of GBM cell growth and migration. Immunoblot analyses showed that ACT-209905 reduced the activation of growth-promoting kinases (p38, AKT1 and ERK1/2), whereas THP-1 cells and conditioned medium caused an activation of these kinases. In addition, ACT-209905 diminished the surface expression of pro-migratory molecules and reduced CD62P-positive GBM cells. In contrast, THP-1 cells increased the ICAM-1 and P-Selectin content of GBM cells which was reversed by ACT-209905. 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S</au><au>Rauch, Bernhard H</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The Putative S1PR1 Modulator ACT-209905 Impairs Growth and Migration of Glioblastoma Cells In Vitro</atitle><jtitle>Cancers</jtitle><date>2023-08-26</date><risdate>2023</risdate><volume>15</volume><issue>17</issue><spage>4273</spage><pages>4273-</pages><issn>2072-6694</issn><eissn>2072-6694</eissn><abstract>Glioblastoma (GBM) is still a deadly tumor due to its highly infiltrative growth behavior and its resistance to therapy. Evidence is accumulating that sphingosine-1-phosphate (S1P) acts as an important tumor-promoting molecule that is involved in the activation of the S1P receptor subtype 1 (S1PR1). Therefore, we investigated the effect of ACT-209905 (a putative S1PR1 modulator) on the growth of human (primary cells, LN-18) and murine (GL261) GBM cells. The viability and migration of GBM cells were both reduced by ACT-209905. Furthermore, co-culture with monocytic THP-1 cells or conditioned medium enhanced the viability and migration of GBM cells, suggesting that THP-1 cells secrete factors which stimulate GBM cell growth. ACT-209905 inhibited the THP-1-induced enhancement of GBM cell growth and migration. Immunoblot analyses showed that ACT-209905 reduced the activation of growth-promoting kinases (p38, AKT1 and ERK1/2), whereas THP-1 cells and conditioned medium caused an activation of these kinases. In addition, ACT-209905 diminished the surface expression of pro-migratory molecules and reduced CD62P-positive GBM cells. In contrast, THP-1 cells increased the ICAM-1 and P-Selectin content of GBM cells which was reversed by ACT-209905. 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| subjects | AKT1 protein Amino acids Cancer Cell culture Cell growth Extracellular signal-regulated kinase Glioblastoma Glioblastoma cells Glioblastoma multiforme Intercellular adhesion molecule 1 Kinases Leukocyte migration Macrophages Medical prognosis Monocytes Motility P-selectin Sphingosine Sphingosine 1-phosphate Tumors |
| title | The Putative S1PR1 Modulator ACT-209905 Impairs Growth and Migration of Glioblastoma Cells In Vitro |
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