title: [Silencing effect of cell-specific RNA interference plasmid pPSMAe/p-shNS-ploy(A) loaded by transgenic vector Tf-PEG-PEI targeting nucleostemin on prostate cancer cells in vitro].
abstract: OBJECTIVE
  To explore the transgenic efficiency of non-viral vector Tf-PEG-PEI and the cell specific silencing effect of plasmid pPSMAe/p-shNS-ploy(A) on prostate cancer cells.
  
  
  METHODS
  Polyethyleneimine (PEI) was modified by using polyethylene glycol and transferrin to synthesize the non-viral vector Tf-PEG-PEI. NS-specific plasmids pPSMAe/p-shNS-ploy(A) and Tf-PEG-PEI were used to transfect prostate cancer LNCap and PC-3 cells. The changes of cell morphology, proliferation ability and cell cycle were studied after down-regulating the NS gene level.
  
  
  RESULTS
  Tf-PEG-PEI was successfully modified. After transfection, the PSMA-expressing LNCaP cells became larger and showed more pseudopodia, having a tendency to differentiate. Their cell proliferation ability was reduced, and the detection of cell cycle showed a decrease of S phase and an increase of G(1) phase after knocking down NS gene. These targets were not changed in non-PSMA-expresing PC-3 cells.
  
  
  CONCLUSIONS
  The non-viral vector Tf-PEG-PEI has a high ability to transfer targeted gene into target cells. The cellular specificity of short-hairpin RNA transcription driven by PSMAe/p is confirmed by silencing NS gene. The use of cell specific promoter may be an effective strategy of gene therapy for prostate cancer.
authors.affiliation: Department of Urology, Second Hospital of Tianjin Medical University & Tianjin Institute of Urology, Tianjin 300211, China.
authors.forename: Ran-lu
authors.initials: RL
authors.lastname: Liu
authors.forename: Wen-yu
authors.initials: WY
authors.lastname: Wang
authors.forename: Zhi-hong
authors.initials: ZH
authors.lastname: Zhang
authors.forename: Yong
authors.initials: Y
authors.lastname: Xu
mesh_terms: D000954:Antigens, Surface / Q000235:genetics* / Q000378:metabolism; D002453:Cell Cycle; D045744:Cell Line, Tumor; D049109:Cell Proliferation; D019204:GTP-Binding Proteins / Q000235:genetics* / Q000378:metabolism; D005822:Genetic Vectors; D043425:Glutamate Carboxypeptidase II / Q000235:genetics* / Q000378:metabolism; D006801:Humans; D008297:Male; D009687:Nuclear Proteins / Q000235:genetics* / Q000378:metabolism; D010957:Plasmids; D011092:Polyethylene Glycols; D011094:Polyethyleneimine / Q000031:analogs & derivatives; D011401:Promoter Regions, Genetic; D011471:Prostatic Neoplasms / Q000473:pathology*; D034622:RNA Interference; D012333:RNA, Messenger / Q000378:metabolism; D034741:RNA, Small Interfering / Q000235:genetics; D014162:Transfection; D014168:Transferrin / Q000235:genetics
chemical_list: D000954:Antigens, Surface; C469949:GNL3 protein, human; D009687:Nuclear Proteins; D012333:RNA, Messenger; D034741:RNA, Small Interfering; D014168:Transferrin; C544016:poly(ethylene glycol)-co-poly(ethyleneimine); D011092:Polyethylene Glycols; D011094:Polyethyleneimine; C473848:FOLH1 protein, human; D043425:Glutamate Carboxypeptidase II; D019204:GTP-Binding Proteins