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Objective To investigate the expression of miRNA-301a-3p in pancreatic cancer and to correlate the expression on invasion , migration and colony formation of pancreatic cancer cells .Methods The expression of miRNA-301a-3p in 20 paired pancreatic cancer tissues and matched adjacent tissues , and pancreatic cancer cell lines and normal pancreatic ductal cells were detected by real -time PCR.miRNA-301a-3p mimics or inhibitors were used to up-regulate or down-regulate the miRNA-301a-3p level in pancre-atic cancer cell lines in order to figure out the effects of miRNA-301a-3p on cell invasion, migration and col-ony formation of pancreatic cancer cells , respectively .Results In pancreatic cancer tissues and cell lines , miRNA-301a-3p was significantly up-regulated when compared with the matched adjacent tissues ( P <0.05) and normal pancreatic ductal cells (P<0.05), respectively.Overexpression or downexpression of miRNA-301a-3p enhanced or suppressed colony formation , invasion and migration abilities of pancreatic cancer cells in vitro.Upregulation of miRNA-301a-3p promoted tumorigenesis in vivo.Conclusion miR-NA-301a-3p might function as an oncogene to promote tumorigenesis in pancreatic cancer .
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Objective To investigate the effect and mechanism of RNAi-mediated STAT3 gene silence on human pancreatic cancer cells growth in vivo. Methods STAT3 shRNA expression vector was stably transfected to SW1990 cells. STAT3 and p-STAT3 protein was examined using Western blot. The growth ability of SW1990 cells in vivo was determined in a subcutaneous tumor model of nude mice. Western blot was performed to detect the protein expression of Bcl-xL and cyclin D1. Results The protein expression of STAT3 and p-STAT3 decreased by 90% and 92% by stable transfection of STAT3 shRNA expressing vectors(P ＜0. 05). Inhibition of STAT3 with RNAi significantly inhibited the growth ability of SW1990 cells in vivo( P ＜ 0. 05 ). The tumor weight significantly decreased( P ＜ 0. 05 ). Moreover, the relative Bcl-xL and cyclinD1 protein expression in SW1990-RNAi cells reduced by 56% and 50% compared with that of the parental SW1990 cells, respectively (P ＜ 0. 05). Conclusions Inhibition of STAT3 with RNAi significantly inhibits the growth ability of pancreatic cancer cells through down-regulating Bcl-xL and cyclin D1.
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Objective: In order to investigate the effects of activating and blocking Stat3 signaling pathway on invasion ability of human pancreatic cancer cells and explore its action mechanism.Methods:Human pancreatic cancer Capan-2 cells were treated with IL-6. SW1990 human pancreatic cancer cells were treated with AG490. Cell proliferation was measured by MTT assay. Western blotting and immunocytochemistry were performed to detect expression of phosphorylated Stat3 (p-Stat3) protein. Real-time fluorogentic quantitative PCR (RFQ-PCR) and Western blotting were used to detect the mRNA and protein expression of VEGF and MMP-2 mRNA, respectively. The invasion abilities of SW1990 and Capan-2 cells were determined by cell invasion assay in vitro. Results:IL-6 stimulated the proliferation of Capan-2 cells (P<0.05), elevated the expression of p-Stat3, increased the mRNA and protein expressions of vascular endothelial growth factor (VEGF) and matrix metalloproteinase 2 (MMP-2) (P<0.05), and enhanced the invasion ability of Capan-2 cells. AG490 inhibited the proliferation of SW1990 cells (P<0.05), down-regulated the expression of p-Stat3, markedly decreased the mRNA and protein expression of VEGF and MMP-2 (P<0.05), and weakened the invasion ability of SW1990 cells. Conclusion:Stat 3 signaling pathway plays an important role in the invasion and metastasis of pancreatic cancer. Stat 3 signaling transduction pathway may provide a novel therapeutic target for the treatment of pancreatic cancer.
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Objective To investigate the effect of RNAi-mediated sTAT3 gene silencing on the invasiveness of human pancreatic cancer cells. Methods STAT3 shRNA expression vector was stably transfected to SW1990 cells.STAT3 mRNA and protein expression were examined using reverse transcription polymerase chain reaction(RT-PCR)and Western blot,respectively.The invasion ability of SW1990 cells was determined by cell invasion assay in vitro.RT-PCR and Westem blot were performed to detect the mRNA and protein expression of the MMP-2 and VEGF,respectively. Results mRNA and protein expression of STAT3 were inhibited significantly by stable transfection of STAT3 shRNA expressing vectors.STAT3 silence with RNAi significantly inhibited the invasion ability of SW1990 cells decreasing protein and mRNA expression of MMP-2 and VEGF in SWl990 cells. Conciusion STAT3 silence with RNAi significantly inhibits the invasion ability of pancreatic cancer cells through down-regulating MMP-2 and VEGF.
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Objectives:To investigate the effects of intravenous LCT or MCT/LCT fat emulsions on the lipid mediators and pancreatic histological changes in ANP rats. Methods:Forty three male SD rats were randomized to groups as follow.Group A～C were without ANP, group A:normal controls, group B:normal rats having received lipid based TPN and group C:operation control(OC) group having received the glucose fluid.Group D～F were with ANP,glucose group,Intralipid group and Lipofundin group.The amylase and prostaglandins in serum were determined in group A.Pancreatic histological examinations were also performed.In group B～F,Amylases or prostaglandins in serum were determined at 4,48 and 72 h, and pancreatic histological examination and pathological scoring were also completed. Results:Intralipid had no effects on serum prostaglandins when it was infused to normal rats.In groups of ANP,intravenous fat emulsion increased the 6 keto PGF 1? ,and PGE 2 concentration in serum at 4 h.Pancreatic hemorrhagic and fat necrosis were significantly reduced in Lipofundin group. Conclusions:Intravenous fat emulsion does not worsen the damages to pancreas in ANP.MCT/LCT fat emulsion is more suitable for patients with ANP.