Pancreatic cancer is one of the most dismal malignancies with the actual 5-year survival ofonly 10 to 20%. Decoy receptor 3 (DcR3) is highly expressed in various cancer cells and plays a significant role in immune suppression and tumor progression. However, how DcR3 expression is modulated in pancreatic cancer cells is enigmatic. The aim of this study was to characterize the expression of DcR3 in pancreatic carcinoma and to evaluate the role of DcR3 in cell proliferation and apoptosis, which may lead to the development of novel treatments for this disease. In the present study, we examined five cell lines including three cell lines from pancreatic cancer (SW1990, Capcan-1 and PANC-1) and two cell lines from colon cancer (HCT116 and RKO) for DcR3 expression by reverse transcriptase-polymerase chain reaction (RT-PCR) and quantitative real time PCR. 3′-(4, 5 dimethyl-thiazol-2-yl)-2, 5-diphenyl tetrazolium bromide (MTT) assay and flow cytometric analysis were used to measure cell proliferation and apoptosis, respectively in the human pancreatic cancer Capan-1 cells. The human pancreatic cancer Capan-1 cell line was first infected with lentivirus-mediated shRNA and then analyzed by real-time PCR, and the results were further confirmed by Western blotting. DcR3 protein in our experimental results showed significant expression among the pancreatic cancer cell lines and their decreased expression by lentivirus-mediated shRNA resulted in the inhibition of cell proliferation and augmentation of apoptosis. In conclusion, these findings suggest that lentivirus-mediated gene therapy targeting DcR3 is a potential and attractive strategy for the treatment of pancreatic cancer.
Key words: Pancreatic cancer, decoy receptor 3 (DcR3), Capcan-1, shRNA.
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