Ad-p53 And The United Radiotherapy On Hela Cells The Role Of Research

The advantage of cancer gene therapy is that it can directly act on the molecular and genetic basis of cancer-specific genes. It becomes a hotspot in the research of cancer now. However, the current therapeutic efficiency of gene therapy is not high enough to lead to complete cancer remission in cancer research. To enhance therapeutic efficiency ofcancer gene therapy, we employed the strategy of combined regimen of therapeutic gene (p53) transfer and chemotherapeutic agent (PDD) administration or radiotherapy. In our experiments with human cervical cancer cell line HeLa cell, which express P53 protein was abnormal, the delivery of p53 was mediated by adenovirus (Ad-p53). The results are as follows:1. In in vitro and in vivo experiments, Ad-p53 can infected HeLa cells successfully and showed therapeutic effects. In vitro, the rate of growth inhibition of HeLa cells treated with Ad-p53 was 61.8%. In vivo, the rate was 54.8%.2. In in vitro and in vivo experiments, Ad-p53 transfer combined cisplatin or radiotherapy administration to HeLa cells could provide substantially stronger therapeutic effects than those provided by single way of administration. In in vitro experiments, Ad-p53 transfer combined cisplatin or radiotherapy caused higher rate of growth inhibition of HeLa cells (87.1% and 85.5%), compared to the growth inhibition induced by single Ad-p53, cisplatin or radiotherapy (61.8%, 50.5% and 44.6%). In in vivo experiments, direct injection of Ad-p53 into HeLa tumors subcutaneously implanted into nude mice, followed by intratumor administration of cisplatin or radiotherapy, caused greater decrease of tumor burden (90.8% and 77.4%) than those caused by the single Ad-p53 injection (54.8%), cisplatin administration (52.4%) or radiotherapy (54.8%). In summary, Ad-p53 for HeLa cells showed enhanced therapeutic efficiency when combined with cisplatin or radiotherapy both in vitro and in vivo.3. Just as the administration of cisplatin or radiotherapy, delivery of Ad-p53 could induce apoptosis of HeLa cells observed from DNA ladder. Cell cycle analysis by FCM demonstrated that all administrations of Ad-p53, cisplatin or radiotherapy singly could arrested HeLa cells in G2-M. Moreover, the administration of Ad-p53 combined cisplatin or radiotherapy, could remarkably arrested HeLa cells in G2-M. The above results may explain the cause of the growth inhibition to HeLa cells by Ad-p53 and explain the reason why Ad-p53 combined with cisplatin or radiotherapy could enhance the therapeutic efficiency in vitro or in vivo for HeLa cells.