title: [Effects of dioscin on apoptosis in pancreatic cancer MiaPaCa-2 cells and its mechanism].
abstract: OBJECTIVE
  The aim of this study was to observe the effects of dioscin on apoptosis and on expression of PRDX1 in pancreatic cancer MiaPaCa-2 cells in vitro.
  
  
  METHODS
  MTT assay was used to detect the growth rate among the medication groups treated with different concentrations of dioscin. The apoptosis rate was determined by annexin V-fluorescein isothiocyanate/propidium iodide double staining and flow cytometry. Western blot analysis was used to assay the expression of PRDX1 and apoptotic proteins in the cells. Reactive oxygen species (ROS) formation was measured by 2'7'-dichlorofluorescein diacetate (DCFH-DA).
  
  
  RESULTS
  Dioscin considerably inhibited the proliferation of MiaPaCa-2 cells in vitro. The inhibitory action was enhanced in a dose-dependent manner. The levels of intracellular ROS detected with DCFH-DA were highly increased after dioscin treatment. The flow cytometry analysis using annexin V-PI staining showed that compared with the apoptotic rate of control group [(3.5 ± 0.7)%], 2.5 µmol/L and 5 µmol/L dioscin induced apoptosis in (28.4 ± 0.9)% and (49.6 ± 2.7)% MiaPaCa-2 cells, and Western blot analysis showed that apoptotic proteins Bax and cleaved caspase-3 expressions were increased and antiapoptotic protein Bcl-2 expression was decreased. In addition, these effects could be blocked by antioxidant N-acetylcysteine (NAC) administration, and the apoptotic rates decreased to (10.8 ± 2.3)% and (18.8 ± 3.0)%, respectively. We further observed the decrease of PRDX1 expression after dioscin treatment. Moreover, after PRDX1 overexpression, dioscin treatment no longer induced high levels of ROS and apoptosis, and the apoptotic rate was decreased to (21.3 ± 5.9)%.
  
  
  CONCLUSIONS
  Dioscin can down-regulate the PRDX1 expression, and then induces ROS-mediated apoptosis in cancer cells.
authors.affiliation: Department of Pancreatic Cancer, Tianjin Medical University Cancer Institute and Hospital, Tianjin Key Laboratory of Cancer Prevention and Treatment, National Clinical Research Center of Cancer, Tianjin 300060, China.
authors.forename: Xiao
authors.initials: X
authors.lastname: Zhao
authors.affiliation: Department of Pancreatic Cancer, Tianjin Medical University Cancer Institute and Hospital, Tianjin Key Laboratory of Cancer Prevention and Treatment, National Clinical Research Center of Cancer, Tianjin 300060, China.
authors.forename: He
authors.initials: H
authors.lastname: Ren
authors.affiliation: Department of Pancreatic Cancer, Tianjin Medical University Cancer Institute and Hospital, Tianjin Key Laboratory of Cancer Prevention and Treatment, National Clinical Research Center of Cancer, Tianjin 300060, China.
authors.forename: Song
authors.initials: S
authors.lastname: Gao
authors.affiliation: Department of Pancreatic Cancer, Tianjin Medical University Cancer Institute and Hospital, Tianjin Key Laboratory of Cancer Prevention and Treatment, National Clinical Research Center of Cancer, Tianjin 300060, China. Email: jihuihao@yahoo.com.
authors.forename: Jihui
authors.initials: J
authors.lastname: Hao
mesh_terms: D017209:Apoptosis / Q000187:drug effects*; D004144:Diosgenin / Q000031:analogs & derivatives* / Q000494:pharmacology; D006801:Humans; D010190:Pancreatic Neoplasms / Q000473:pathology*; D054464:Peroxiredoxins / Q000187:drug effects*; D017382:Reactive Oxygen Species / Q000378:metabolism
chemical_list: D017382:Reactive Oxygen Species; C019357:dioscin; C515940:PRDX1 protein, human; D054464:Peroxiredoxins; D004144:Diosgenin