Expression of TP53, BCL-2, and VEGFA Genes in Esophagus Carcinoma and its Biological Significance

摘要

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 [i]de novo[/i] vascular formation while B-cell lymphoma-2 ([i]BCL-2[/i]) gene exerts a tumor-suppressing effect. The prominent expression of [i]VEGFA[/i] and [i]BCL-2[/i] genes, along with the most famous tumor-suppressor gene, [i]TP53[/i], raise the possibly of gene interaction. This study therefore investigated the effect and correlation of [i]TP53[/i], [i]BCL-2[/i], and [i]VEGFA[/i] genes on cell proliferation and apoptosis of esophagus carcinoma. MATERIAL AND 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 [i]TP53[/i], [i]BCL-2[/i] and [i]VEGFA[/i] 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 [i]TP53[/i], [i]BCL-2[/i], and [i]VEGFA[/i] genes may participate in the proliferation of esophagus cancer cells in a synergistic manner.