The prognosis of pancreatic cancer is still very poor. proliferation, increasing cell apoptosis and regulating cell cycle as well. tests proven that the mean quantity and pounds of subcutaneous xenografts in naked rodents extracted from Capan-2 cells transfected with COX-2 siRNA had been considerably reduced. COX-2 siRNA could lessen the development of Capan-2 pancreatic tumor cells and also reduce the tumorigenicity of buy ARQ 197 Capan-2 cells, implicating a fresh potential restorative focus on in pancreatic tumor. reported that the appearance of COX-2 mRNA in pancreatic tumor cells was higher by 60 instances than that in surrounding non-tumor pancreatic cells (12). The appearance of COX-2 was remarkably improved in some human being pancreatic tumor cell lines (13). Nevertheless, the system is unclear still. Our earlier research discovered that the high appearance of COX-2 was related to the high appearance of catalyst element of telomerase, hTERT (3,4). That indicated that COX-2 Rabbit Polyclonal to RRAGA/B performed a important part in the tumorigenesis, metastasis and advancement of pancreatic tumor, which suggests that COX-2 was one of the essential focuses on of gene therapy in pancreatic tumor. The COX-2 inhibitor could lessen expansion of pancreatic tumor cells via down-regulation of the appearance of COX-2. Nevertheless, why perform we apply RNAi focusing on COX-2 gene to lessen proliferation of pancreatic cancer cells? A great deal of epidemiological data showed that although long-term use of NSAID may decrease the risk of cancer, it may lead to complications of the gastrointestinal tract, renal, cardiovascular and cerebrovascular system. In addition, the inhibition rate of cell proliferation on pancreatic cancer by the COX-2 inhibitor was limited with a range of 40C62% depending on the dosage of COX-2 inhibitor (14,15). However, the inhibition rate of cell proliferation was increased only by about 10% when the dosage of COX-2 inhibitor was doubled (16). Moreover, the risk of cardiovascular events may be increased when the dosage of COX-2 inhibitor was increased. COX-2 selective inhibitors or COX-2 non-selective inhibitors applied in the previous studies all post-translationally regulated COX-2 expression with a dose-dependent COX-2 inhibition effect and limited inhibition efficiency. As the COX-2 inhibitor does not result in specific inhibition, it more or less inhibited COX-1 which maintained the normal physiological function in body. Therefore, it may increase the risk of hypertension and cardiovascular diseases (17). The safety of COX-2 inhibitor in anticancer research needs further clinical investigation. RNAi could be utilized to promote cell apoptosis, hinder expansion of tumor cells, intrusion and metastasis of tumor and medication level of resistance by suppressing the phrase of oncogene and genetics that are related to carcinogenesis and advancement (3,4). RNAi offers become a effective device in tumor study as the benefit buy ARQ 197 can be got by it of great dependability, high specificity, low cytotoxicity and lengthy and solid impact therefore on. Nevertheless, the crucial stage of its effective software can be that the high effectiveness silencing series (silencing price >70%) and high-throughput vector could become tested in progress. Our data demonstrated that liposome Lipofactamine 2000 got as high as 96.47% of a transfection rate in Capan-2 cancer cells. In the in the meantime, COX-2 siRNA006, the most effective silencing series was tested from six COX-2 siRNAs sequences. COX-2 siRNA006 focusing on COX-2 gene was utilized to investigate its impact on cell proliferation, cell cycle and cell apoptosis in Capan-2 pancreatic cancer cells. We found that there was no significant difference in cell viability among different groups at 24 h after transfection. Cell viability of Capan-2 cells in the COX-2 siRNA006 group was significantly decreased at 48 h after transfection. buy ARQ 197 The inhibition rate of cell proliferation was 35.48 and 56.32% respectively at 48 and 72 h after transfection. The cells in G0/G1 phase were significantly increased as the culture time of cells transfected with COX-2 siRNA006 was increased. However, the cells in the S phase were significantly decreased. The apoptotic cells were increased as the culture time of cells transfected with COX-2 siRNA006 was increased. To further verify the effect of COX-2 siRNA silencing COX-2 gene on cell growth of Capan-2 individual pancreatic tumor cells, Capan-2 cells transfected with COX-2 siRNA had been subcutaneously inoculated into BALB/c-nu/nu naked rodents buy ARQ 197 to check out the impact of COX-2 siRNA on tumorigenicity of Capan-2 cells. Our data demonstrated that COX-2 siRNA could considerably hinder the tumorigenicity of Capan-2 individual pancreatic tumor cells in naked rodents. The above stated data and.