The Malignant Phenotypic Reversion Of Esophageal Carcinoma Cells Transfected By P53 And P16 Gene

Balancing the rates of cell proliferation and cell death is important in maintaining normal tissue homeostasis. Disruption of this balance involving the activation of oncogenes and inactivation of antioncogenes may be a major factor in the multistep process of tumorigenesis. The most mutant p53 gene in human tumor and recently reported p16 gene (multiple tumor gene 1) related to the cell cycle control. They take play an important role in the tumor progression. The present study is designed to investigate the malignet phenotype reversion of esophageal cell line transfected p53 and p16 gene,and to provide a scientific slue for genotherapy of esophageal carcinoma. On the other hand, It is designed to observe the effect of antisense p53 of the tunorgenesis in the NIH 3T3 cell and Rat-1 cell by blocking expression of normal wild-type p53 .Part 1: The potential value of wtp53 gene in the treatment ofesophageal carcinoma1. Analysis of p53 gene in the esophageal carcinoma cells of human fetus induced by NMBzA.1). Southern blot assay and PCR analysis showed that p53 gene deleted in the esophageal carcinoma cells of human fetus induced by NMBZA(NEC).2). Northern blot assay showed that there was not expression of p53 gene in the esophageal carcinoma cells of human fetus induced by NMBzA.2. Inhibition of . the esophageal carcinoma cells transfected by wild-type p53 gene1). Northern blotting showed that the NEC cell with transfected wild-type p53 presents the exogenous 1.8 kb p53 mRNA.