Experimental Study On Combination Of Adenovirus-p53 With Celecoxib And Cisplatin In Human Lung Adenocarcinoma Cell Lines

The most common cancer in the world is lung cancer, lung cancer is the leading cause of death from cancer in most developed nations. Unfortunately, the overall survival for lung cancer with conventional treatments (chemotherapy, radiotherapy, and surgery) is less than 15% in the world. In the past few years, follow the continuously studying of molecule-biology, bio-molecule target treatment has been becoming a significant means of the lung cancer treated.Studies revealed, the p53 tumor suppressor protein is crucial to the regulation of the cell cycle and control of apoptosis. Removal of p53 function results in genetic instability and the inability of cells to go through apoptosis when exposed to chemotherapy or radiation therapy. The p53 gene is mutated in 50% to 70% of patients with lung cancer. Additionally, in a large proportion of cases in which there is no mutation, p53 is inactivated through binding by high levels of Mdm-2 protein,or is functionally inactive because downstream gene such as the proapoptotic bcl-2 family members that p53 transactivates are mutated or transcriptionally inactive. It has been reported that using adenoviral mediated p53 gene transfer to lung cancer cells can enhance the cytotoxic effect of anti-cancer drugs, which leading to an improvement of lung cancer chemotherapy.