Objective: To investigate the biological effects of wtp53 expression on the growth rate and apoptosis of human pancreatic carcinoma.
Methods: The Ad5CMVwtp53 a recombinant replication-deficient adenoviral vector containing a human CMV promoter, a human wild-type p53 and the SV40 polyadenylation signal was amplified in 293 packaging cells. The pancreatic carcinoma cell line (PC-2), carrying a mutation of p53 gene at codon 240, was transfected using Ad5CMV wtp53 and the control adenoviral vector Ad5pXJ.
Results: The cells transfected with Ad5CMV wtp53 showed that presence and expression of wtp53 gene were demonstrated using PCR and immunoprecipitation, that growth rate and 3H-TdR incorporation rate were decreased. The restoration of wtp53 encoded protein in PC-2 cells induced apoptosis assessed by in situ TUNEL apoptosis, flow cytometry, DNA agarose gel electrophoresis analyses, whereas noninfected cells or the cells infected with control virus didn't show these changes.
Conclusion: Replication-deficient adenoviral vector is an efficient vector in transferring wtp53 gene and antitumor therapy using the p53 gene is a valuable method in inhibiting pancreatic cancer cells growth by inducing apoptosis.