title: Expression of TP53, BCL-2, and VEGFA Genes in Esophagus Carcinoma and its Biological Significance.
abstract: BACKGROUND
  The pathogenesis of esophagus carcinoma involves a cascade process consisting of multiple factors and accumulation of gene mutations. It is known that vascular endothelial growth factor (VEGF) mainly regulates de novo vascular formation while B-cell lymphoma-2 (BCL-2) gene exerts a tumor-suppressing effect. The prominent expression of VEGFA and BCL-2 genes, along with the most famous tumor-suppressor gene, TP53, raise the possibly of gene interaction. This study therefore investigated the effect and correlation of TP53, BCL-2, and VEGFA genes on cell proliferation and apoptosis of esophagus carcinoma.
  
  
  METHODS
  A total of 30 male rats were prepared by subcutaneous injection of methyl-benzyl-nitrosamine (MBNA) to induce esophagus cancer, along with 30 controlled rats which received saline instead. After 4, 10, 20, or 30 weeks, rats were sacrificed to observe the morphological changes of esophageal mucosa. Cell apoptosis was quantified by terminal deoxynucleotidyl transferase-mediated dUTP nick-end-labeling (TUNEL) assay. Immunohistochemical (IHC) staining was employed to examine the expression of TP53, BCL-2 and VEGFA genes.
  
  
  RESULTS
  With the progression of cancer, pathological damages of esophageal tissue aggravated while the cancer cell apoptosis gradually decreased compared to controlled animals. Protein levels of p53, Bcl-2, and VEGF in the model group were significantly elevated at each time point. Positive correlations existed between p53 and Bcl-2 or VEGF.
  
  
  CONCLUSIONS
  Abnormally elevated expression of TP53, BCL-2, and VEGFA genes may participate in the proliferation of esophagus cancer cells in a synergistic manner.
authors.affiliation: Cancer Center, The Second Hospital of Shandong University, Jinan, Shandong, China (mainland).
authors.forename: Wei
authors.initials: W
authors.lastname: Wei
authors.affiliation: Department of Rehabilitation Medicine, Qilu Hospital of Shandong University, Jinan, Shandong, China (mainland).
authors.forename: Yanqin
authors.initials: Y
authors.lastname: Wang
authors.affiliation: Cancer Center, The Second Hospital of Shandong University, Jinan, Shandong, China (mainland).
authors.forename: Xiaoming
authors.initials: X
authors.lastname: Yu
authors.affiliation: Cancer Center, The Second Hospital of Shandong University, Jinan, Shandong, China (mainland).
authors.forename: Lan
authors.initials: L
authors.lastname: Ye
authors.affiliation: Cancer Center, The Second Hospital of Shandong University, Jinan, Shandong, China (mainland).
authors.forename: Yuhua
authors.initials: Y
authors.lastname: Jiang
authors.affiliation: Department of Radiotherapy, Qilu Hospital of Shandong University, Jinan, Shandong, China (mainland).
authors.forename: Yufeng
authors.initials: Y
authors.lastname: Cheng
mesh_terms: D000818:Animals; D017209:Apoptosis; D001471:Barrett Esophagus / Q000378:metabolism; D002277:Carcinoma / Q000378:metabolism*; D049109:Cell Proliferation; D004128:Dimethylnitrosamine / Q000031:analogs & derivatives; D004938:Esophageal Neoplasms / Q000378:metabolism*; D020869:Gene Expression Profiling; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D007150:Immunohistochemistry; D020287:In Situ Nick-End Labeling; D008297:Male; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism*; D051560:Proto-Oncogene Proteins c-bcl-6 / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism*; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism*
chemical_list: D019253:Proto-Oncogene Proteins c-bcl-2; D051560:Proto-Oncogene Proteins c-bcl-6; D016159:Tumor Suppressor Protein p53; D042461:Vascular Endothelial Growth Factor A; C467498:vascular endothelial growth factor A, rat; C014707:nitrosobenzylmethylamine; D004128:Dimethylnitrosamine