Your browser doesn't support javascript.
loading
Sphingosine 1-phosphate signaling through its receptor S1P5 promotes chromosome segregation and mitotic progression.
Andrieu, Guillaume; Ledoux, Adeline; Branka, Sophie; Bocquet, Magalie; Gilhodes, Julia; Walzer, Thierry; Kasahara, Kousuke; Inagaki, Masaki; Sabbadini, Roger A; Cuvillier, Olivier; Hatzoglou, Anastassia.
Afiliación
  • Andrieu G; CNRS, Institut de Pharmacologie et de Biologie Structurale, 31400 Toulouse, France.
  • Ledoux A; Université de Toulouse, Université Paul Sabatier, 31400 Toulouse, France.
  • Branka S; Equipe Labellisée Ligue Contre le Cancer, 31400 Toulouse, France.
  • Bocquet M; CNRS, Institut de Pharmacologie et de Biologie Structurale, 31400 Toulouse, France.
  • Gilhodes J; Université de Toulouse, Université Paul Sabatier, 31400 Toulouse, France.
  • Walzer T; Equipe Labellisée Ligue Contre le Cancer, 31400 Toulouse, France.
  • Kasahara K; CNRS, Institut de Pharmacologie et de Biologie Structurale, 31400 Toulouse, France.
  • Inagaki M; Université de Toulouse, Université Paul Sabatier, 31400 Toulouse, France.
  • Sabbadini RA; Equipe Labellisée Ligue Contre le Cancer, 31400 Toulouse, France.
  • Cuvillier O; CNRS, Institut de Pharmacologie et de Biologie Structurale, 31400 Toulouse, France.
  • Hatzoglou A; Université de Toulouse, Université Paul Sabatier, 31400 Toulouse, France.
Sci Signal ; 10(472)2017 Mar 28.
Article en En | MEDLINE | ID: mdl-28351953
Sphingosine kinase 1 (SphK1) promotes cell proliferation and survival, and its abundance is often increased in tumors. SphK1 produces the signaling lipid sphingosine 1-phosphate (S1P), which activates signaling cascades downstream five G protein-coupled receptors (S1P1-5) to modulate vascular and immune system function and promote proliferation. We identified a new function of the SphK1-S1P pathway specifically in the control of mitosis. SphK1 depletion in HeLa cells caused prometaphase arrest, whereas its overexpression or activation accelerated mitosis. Increasing the abundance of S1P promoted mitotic progression, overrode the spindle assembly checkpoint (SAC), and led to chromosome segregation defects. S1P was secreted through the transporter SPNS2 and stimulated mitosis by binding to and activating S1P5 on the extracellular side, which then activated the intracellular phosphatidylinositol 3-kinase (PI3K)-AKT pathway. Knockdown of S1P5 prevented the S1P-induced spindle defect phenotype. RNA interference assays revealed that the mitotic kinase Polo-like kinase 1 (PLK1) was an important effector of S1P-S1P5 signaling-induced mitosis in HeLa cells. Our findings identify an extracellular signal and the downstream pathway that promotes mitotic progression and may indicate potential therapeutic targets to inhibit the proliferation of cancer cells.
Asunto(s)

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Esfingosina / Lisofosfolípidos / Transducción de Señal / Segregación Cromosómica / Receptores de Lisoesfingolípidos / Mitosis Tipo de estudio: Prognostic_studies Límite: Animals / Humans Idioma: En Revista: Sci Signal Asunto de la revista: CIENCIA / FISIOLOGIA Año: 2017 Tipo del documento: Article País de afiliación: Francia Pais de publicación: Estados Unidos

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Esfingosina / Lisofosfolípidos / Transducción de Señal / Segregación Cromosómica / Receptores de Lisoesfingolípidos / Mitosis Tipo de estudio: Prognostic_studies Límite: Animals / Humans Idioma: En Revista: Sci Signal Asunto de la revista: CIENCIA / FISIOLOGIA Año: 2017 Tipo del documento: Article País de afiliación: Francia Pais de publicación: Estados Unidos