title: [Multiple inhibitory mechanisms of wild-type p16 gene transfer into human bladder cells by retroviral vector].
abstract: OBJECTIVE
  To investigate the inhibitory mechanisms of wild-type p16 gene transfer into human bladder cancer cells with or without endogenous p16 gene expression.
  
  
  METHODS
  p16 recombinant retrovirus vector was constructed and transfected in human bladder cancer cell EJ and 253J. Northern blot analysis and immunocytochemistry were used to detect the expression of exogenous p16 gene. Flow cytometry analysis was used to detect tumor cell cycle. Electronic microscope and in situ labelling apoptotic DNA fragment detection (TUNEL) was used to detect tumor cell apoptosis after gene transfection. Tumorigenicity was observed in nude mice.
  
  
  RESULTS
  The growth rate of the transfected EJ cells was significantly retarded, the majority of transfected EJ cells were arrested on G(0) + G(1) phases of cell cycle, tumorigenicity of the transfected cells was reduced on nude mice. H-ras gene expression in transfected EJ cells reduced as compared with non-transfection. Apoptotic cells were observed in transgenic 253J cells.
  
  
  CONCLUSIONS
  Malignant proliferation of bladder cancer cells can be inhibited by exogenous p16 gene transfection via different molecular pathway.
authors.affiliation: Tianjin Institute of Urological Surgery, Tianjin 300211.
authors.forename: Y
authors.initials: Y
authors.lastname: Wu
authors.forename: T
authors.initials: T
authors.lastname: Ma
authors.forename: H
authors.initials: H
authors.lastname: Wu
authors.forename: W
authors.initials: W
authors.lastname: Zhang
authors.forename: C
authors.initials: C
authors.lastname: Wu
mesh_terms: D000818:Animals; D017209:Apoptosis; D002453:Cell Cycle; D045744:Cell Line, Tumor; D019942:Genes, p16; D005822:Genetic Vectors; D006801:Humans; D051379:Mice; D008807:Mice, Inbred BALB C; D008819:Mice, Nude; D012190:Retroviridae / Q000235:genetics; D014162:Transfection; D001749:Urinary Bladder Neoplasms / Q000235:genetics / Q000473:pathology*