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The majority of patients with pancreatic cancer are resistant to gemcitabine.One of the mechanisms involved is the anti-apoptotic ability of these cells. Themedian lethal dose (LD50) of gemcitabine for PANC-1 cells was higher than thatfor Mia PaCa-2 cells and the former had higher nuclear factor-κB (NF-κB) and X-linkedinhibitor of apoptosis protein (XIAP) levels. NF-κB contributes to the inhibitionof apoptosis by the downregulation of downstream genes, such as XIAP and Bcl-2and it confers chemoresistance. The two cell lines were infected with NF-κB p65small interfering RNA (siRNA). p65 protein was effectively downregulated accompaniedby the downregulation of XIAP protein. The combination treatment with gemcitabineand p65 siRNA increased the apoptotic rates in both cell lines; however, thiswas not sufficient. XIAP is involved in apoptosis to a greater extent compatedto Bcl-2. XIAP may serve as another factor affecting the sufficiency of chemotherapy.XIAP siRNA was designed to knockdown XIAP. Mia PaCa-2 and PANC-1 cells were co-infectedwith XIAP siRNA and p65 siRNA. XIAP and p65 proteins were effectively downregulatedand the gemcitabine-induced apoptotic rates were significantly increased. Theseresults suggest that XIAP and NF-κB are two important factors conferring the chemoresistanceof pancreatic cancer cells, and that their downregulation via RNAi effectivelyenhances the chemosensitivity of pancreatic cancer cells to gemcitabine.

Double inhibition of NF-κB and XIAP via RNAi enhances the sensitivity of pancreatic cancer cells to gemcitabine