RESUMO
To observe the expression of human wild-type p53, B7-1 and GM-CSF genes mediated by recom-binant adenovirus and their effects of inducing apoptosis on lung cancer cells. Methods; Human wild-type p53, B7-1 and GM-CSF genes were transfected into lung cancer cells mediated by recombinant adenovirus. The expression products of these genes were detected by immunohistochemistry assay, flow cytometric analysis and ELISA. Cell growth assay was carried out by counting alive cells after trypan blue exclusion. Cell apoptosis was detected by TdT assay of DNA fragmentation . Results: The multi-genes could be efficiently expressed in lung cancer cells mediated by recombinant adenovirus, which could suppress lung cancer cell growth and induce their apoptosis. Conclusion: These results suggest the feasibility of muti-gene therapy for lung cancer.
RESUMO
Objective To study the effect of a recombinant adenovirus carrying p53 gene, B7 1 gene and GM CSF (BB 102) on the nude mice transferred with laryngeal carcinoma. Methods Nude mice model bearing laryngocarcinoma was established using human laryngeal squamous carcinoma cell line (Hep 2). Large amounts of recombinant adenovirus (BB 102) were injected into the tumor. Changes in carcinoma treated with recombinant BB 102 adenovirus were observed under light and electron microscopes. Results The difference between experimental and control groups was statistically significant. The morphology of cells infected with BB 102 was analyzed for evidence of apoptosis by transmission electron microscopy. It has been shown that wild type P53 protein can inhibit cell growth and induce apoptosis, while B7 1 and GM CSF have no such effects. Conclusions The results showed that recombinant adenovirus BB 102 has significant efficacy in suppressing tumor cell growth and in inducing their apoptosis, suggesting that BB 102 might be developed into a therapeutic agent in clinical therapy of laryngeal carcinoma