title: Sorafenib inhibits growth, migration, and angiogenic potential of ectopic endometrial mesenchymal stem cells derived from patients with endometriosis.
abstract: OBJECTIVE
  To characterize the proliferation, migration, and angiogenic properties of mesenchymal stem cells (MSC) from ectopic and eutopic endometrial tissue and to investigate the effect of the tyrosine kinase inhibitor sorafenib.
  
  
  METHODS
  In vitro studies.
  
  
  METHODS
  University hospital and research center.
  
  
  METHODS
  Patients receiving surgical treatment of endometriosis (n = 4) and control patients without endometriosis (n = 2) undergoing surgery for benign gynecologic diseases.
  
  
  METHODS
  Mesenchymal stem cell lines were isolated from ectopic and eutopic endometrial tissue, and sorafenib was administered to them.
  
  
  METHODS
  Proliferation, migration, invasion of endometrial MSC, and expression of ezrin, vascular endothelial growth factor, and hypoxia-inducible factor-1α (HIF-1α) were measured.
  
  
  RESULTS
  Ectopic endometrial MSC from patients with endometriosis showed a higher proliferation, migration, and angiogenic ability than eutopic MSC from the same patient or control MSC from patients without endometriosis. Sorafenib reduced the proliferation, motility, ezrin phosphorylation, vascular endothelial growth factor release, and HIF-1α expression of ectopic MSC.
  
  
  CONCLUSIONS
  The increased proliferative, migratory, and angiogenic phenotype of ectopic MSC may be reverted by treatment with sorafenib. Targeting of the MSC population involved in sustaining the ectopic lesions might be useful in eradicating endometriotic implants.
authors.affiliation: Department of Internal Medicine, Molecular Biotechnology Center, University of Torino, Torino, Italy.
authors.forename: Aldo
authors.initials: A
authors.lastname: Moggio
authors.forename: Giulia
authors.initials: G
authors.lastname: Pittatore
authors.forename: Paola
authors.initials: P
authors.lastname: Cassoni
authors.forename: Gian Luigi
authors.initials: GL
authors.lastname: Marchino
authors.forename: Alberto
authors.initials: A
authors.lastname: Revelli
authors.forename: Benedetta
authors.initials: B
authors.lastname: Bussolati
mesh_terms: D000328:Adult; D020533:Angiogenesis Inhibitors / Q000008:administration & dosage; D001557:Benzenesulfonates / Q000008:administration & dosage*; D002465:Cell Movement / Q000187:drug effects; D049109:Cell Proliferation / Q000187:drug effects; D002478:Cells, Cultured; D004715:Endometriosis / Q000188:drug therapy* / Q000473:pathology*; D004717:Endometrium / Q000187:drug effects* / Q000473:pathology; D005260:Female; D006801:Humans; D059630:Mesenchymal Stem Cells / Q000187:drug effects* / Q000473:pathology; D008875:Middle Aged; D009389:Neovascularization, Pathologic / Q000188:drug therapy* / Q000517:prevention & control*; D009536:Niacinamide / Q000031:analogs & derivatives; D010671:Phenylurea Compounds; D047428:Protein Kinase Inhibitors / Q000008:administration & dosage; D011725:Pyridines / Q000008:administration & dosage*; D000077157:Sorafenib; D016896:Treatment Outcome; D055815:Young Adult
chemical_list: D020533:Angiogenesis Inhibitors; D001557:Benzenesulfonates; D010671:Phenylurea Compounds; D047428:Protein Kinase Inhibitors; D011725:Pyridines; D009536:Niacinamide; D000077157:Sorafenib