title: Erucylphosphocholine shows a strong anti-growth activity in human endometrial and ovarian cancer cells.
abstract: OBJECTIVE
  A membrane-targeted, lipophilic ether lipid of synthetic phospholipid analog, erucylphosphocholine (ErPC) induces apoptosis in some lines of human tumor cells. We investigated the effect of ErPC on three endometrial cancer cell lines, two ovarian cancer cell lines, and normal human endometrial epithelial cells.
  
  
  METHODS
  Endometrial and ovarian cancer cells were treated with various concentrations of ErPC, and its effect on cell growth, cell cycle, apoptosis, and related measurements was investigated.
  
  
  RESULTS
  The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay showed that all endometrial and ovarian cancer cell lines were sensitive to the growth-inhibitory effect of ErPC, although normal endometrial epithelial cells were viable after treatment with the same doses of ErPC that induced growth inhibition in endometrial and ovarian cancer cells. Cell cycle analysis indicated that their exposure to ErPC decreased the proportion of cells in the S-phase and increased the proportion in the G2/M phases of the cell cycle. Induction of apoptosis was confirmed by annexin V staining of externalized phosphatidylserine and loss of the transmembrane potential of mitochondria. This induction occurred in concert with altered expression of genes related to cell growth, malignant phenotype, and apoptosis.
  
  
  CONCLUSIONS
  These results suggest that the anticancer activity of ErPC may occur with higher sensitivity of cancer cells compared with normal healthy cells, when using low concentration, rising hopes that ErPC may become a useful adjuvant therapy for endometrial and ovarian cancers.
authors.affiliation: Department of Obstetrics and Gynecology, Oita University Faculty of Medicine, 1-1 Idaigaoka, Hasama-machi, Yufu-shi, Oita 879-5593, Japan.
authors.forename: Noriyuki
authors.initials: N
authors.lastname: Takai
authors.forename: Tami
authors.initials: T
authors.lastname: Ueda
authors.forename: Kaei
authors.initials: K
authors.lastname: Nasu
authors.forename: Hisashi
authors.initials: H
authors.lastname: Narahara
mesh_terms: D017209:Apoptosis / Q000187:drug effects; D053453:Caspase 9 / Q000378:metabolism; D002453:Cell Cycle / Q000187:drug effects; D018797:Cell Cycle Proteins / Q000096:biosynthesis; D048708:Cell Growth Processes / Q000187:drug effects; D045744:Cell Line, Tumor; D019926:Cyclin B / Q000096:biosynthesis; D056744:Cyclin B1; D004305:Dose-Response Relationship, Drug; D016889:Endometrial Neoplasms / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D053078:Membrane Potential, Mitochondrial / Q000187:drug effects; D010051:Ovarian Neoplasms / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D010767:Phosphorylcholine / Q000031:analogs & derivatives* / Q000494:pharmacology; D017346:Protein Serine-Threonine Kinases / Q000096:biosynthesis; D011518:Proto-Oncogene Proteins / Q000096:biosynthesis; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000096:biosynthesis; D000097869:Polo-Like Kinase 1
chemical_list: D053453:Caspase 9; D018797:Cell Cycle Proteins; D019926:Cyclin B; D056744:Cyclin B1; D010767:Phosphorylcholine; D017346:Protein Serine-Threonine Kinases; D011518:Proto-Oncogene Proteins; D019253:Proto-Oncogene Proteins c-bcl-2; D000097869:Polo-Like Kinase 1; C534699:CCNB1 protein, human; C075010:erucylphosphocholine