title: Reversing effect of exogenous WWOX gene expression on malignant phenotype of primary cultured lung carcinoma cells.
abstract: BACKGROUND
  Whether WW domain containing oxidoreductase (WWOX) gene is a tumor-suppressor is still controversial. Some researchers found that the transcription of the WWOX gene was lacking not only in tumor tissues but also in non-tumorous tissues and sometimes in normal tissues. Hence it is important to explore the role of the expression of the exogenous WWOX gene in the proliferation and apoptosis of primary cultured lung carcinoma cells.
  
  
  METHODS
  Lipofection technique was used to determine primary cultured lung carcinoma cells containing the highly expressed exogenous WWOX gene and primary cultured cells with vectors as controls. An animal model of lung cancer was made by subcutaneous implantation of tumor cells into nude mice. RT-PCR, Western blotting, flow cytometry, and TUNEL were used to detect the transcription, expression of the exogenous gene and the effect of the expression of targeted genes on the proliferation and apoptosis of the primary cultured lung carcinoma cells.
  
  
  RESULTS
  The growth, clone formation rate (CFR) ((5.33 +/- 1.53)%) of the primary lung cancer cells transfected with the WWOX gene, tumor size and weight were significantly lower than those of the non-transfected lung cancer cells (CFR: (14.33 +/- 1.53)%) and the primary lung cancer cells transfected with blank plasmids (CFR: (11.00 +/- 1.73)%, P < 0.05). The apoptosis level of primary lung cancer cells transfected with the WWOX gene ((40.72 +/- 5.20)%) was significantly higher than that of the non-transfected lung cancer cells ((2.76 +/- 0.02)%) and the primary lung cancer cells transfected with blank plasmids ((2.72 +/- 0.15)%, P < 0.05).
  
  
  CONCLUSIONS
  The expression of the exogenous WWOX gene can significantly inhibit the proliferation of lung cancer cells and induce their apoptosis, suggesting that the WWOX gene possesses tumor-suppressing effect.
authors.affiliation: Department of Chest Internal Medicine, Tianjin Chest Hospital, Tianjin 300051, China. longfengcao@tom.com
authors.forename: Yu-long
authors.initials: YL
authors.lastname: Zhou
authors.forename: Yue-chuan
authors.initials: YC
authors.lastname: Li
authors.forename: Feng
authors.initials: F
authors.lastname: Shou
authors.forename: Chang-qi
authors.initials: CQ
authors.lastname: Liu
authors.forename: Yong
authors.initials: Y
authors.lastname: Pu
authors.forename: Hua
authors.initials: H
authors.lastname: Tang
mesh_terms: D000818:Animals; D017209:Apoptosis; D002277:Carcinoma / Q000473:pathology*; D045744:Cell Line, Tumor; D049109:Cell Proliferation; D006801:Humans; D008175:Lung Neoplasms / Q000473:pathology*; D051379:Mice; D008807:Mice, Inbred BALB C; D010088:Oxidoreductases / Q000235:genetics* / Q000502:physiology; D010641:Phenotype; D025521:Tumor Suppressor Proteins / Q000235:genetics* / Q000502:physiology; D000074584:WW Domain-Containing Oxidoreductase
chemical_list: D025521:Tumor Suppressor Proteins; D010088:Oxidoreductases; D000074584:WW Domain-Containing Oxidoreductase; C486071:WWOX protein, human