title: Growth inhibitory effect of D-allose on human ovarian carcinoma cells in vitro.
abstract: BACKGROUND
  D-allose is a rare sugar found in nature and, because of its very limited amount and of the high cost associated with its synthesis, its physiological functions remain virtually unknown. The aim of the current study was to investigate the effect of D-allose on the proliferation of human ovarian carcinoma cells in vitro.
  
  
  METHODS
  Human ovarian carcinoma cells (OVCAR-3 cell line) were exposed to rare sugars including D-allose, D-altrose, D-psicose and D-talitol. Cell growth was evaluated by MTT assay. Cell cycle analysis was carried out by flow cytometric assay. The expression of cell cycle regulatory proteins was determined by Western blot analysis. TUNEL assay was employed for the detection of apoptotic cells.
  
  
  RESULTS
  D-allose had a significant inhibitory effect on ovarian cancer cell proliferation in a dose-dependent manner, and caused a moderate G2/M arrest in the cell cycle, up-regulation of Cdk inhibitors p21 and p27 levels, and the induction of apoptosis in OVCAR-3 cells.
  
  
  CONCLUSIONS
  Our results show, for the first time, that D-allose inhibits the growth of ovarian carcinoma cells in vitro. Although the exact mechanisms remain unclear, these findings suggest that D-allose possesses a novel inhibitory property on ovarian carcinoma cell proliferation, and may represent a new class of compounds with possible therapeutic potential.
authors.affiliation: Department of Cell Physiology, Faculty of Medicine, Kagawa University, Kagawa, Japan.
authors.forename: Li
authors.initials: L
authors.lastname: Sui
authors.forename: Youyi
authors.initials: Y
authors.lastname: Dong
authors.forename: Yasuo
authors.initials: Y
authors.lastname: Watanabe
authors.forename: Fuminori
authors.initials: F
authors.lastname: Yamaguchi
authors.forename: Naoya
authors.initials: N
authors.lastname: Hatano
authors.forename: Ken
authors.initials: K
authors.lastname: Izumori
authors.forename: Masaaki
authors.initials: M
authors.lastname: Tokuda
mesh_terms: D000230:Adenocarcinoma / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D017209:Apoptosis / Q000187:drug effects; D002453:Cell Cycle / Q000187:drug effects; D018797:Cell Cycle Proteins / Q000096:biosynthesis; D048708:Cell Growth Processes / Q000187:drug effects; D045744:Cell Line, Tumor; D050759:Cyclin-Dependent Kinase Inhibitor p21; D050760:Cyclin-Dependent Kinase Inhibitor p27; D004305:Dose-Response Relationship, Drug; D005260:Female; D005632:Fructose / Q000494:pharmacology; D005947:Glucose / Q000494:pharmacology*; D006801:Humans; D010051:Ovarian Neoplasms / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D013402:Sugar Alcohols / Q000494:pharmacology; D025521:Tumor Suppressor Proteins / Q000096:biosynthesis
chemical_list: C493956:CDKN1A protein, human; D018797:Cell Cycle Proteins; D050759:Cyclin-Dependent Kinase Inhibitor p21; D013402:Sugar Alcohols; D025521:Tumor Suppressor Proteins; D050760:Cyclin-Dependent Kinase Inhibitor p27; C003243:psicose; D005632:Fructose; C042890:altritol; C002055:allose; D005947:Glucose