Circular RNAs(CircRNAs)are a class of non-coding RNAs with a covalently closed-loop structure,high stability,and tissue specificity,with the production mechanisms different from linear RNAs.Recent studies have discovered that some CircRNAs can encode proteins via cap-independent translation mechanisms such as internal ribosome entry site,N6-methyladenosine,and rolling loop translation.The encoded proteins regulate homologous linear proteins or downstream signaling pathways via protein bait or other mecha-nisms,thereby exerting biological functions.Studies have shown that CircRNAs play a role in various diseases,especially in tumor progression,proliferation,invasion,and metastasis and immune regulation.Therefore,by elucidating the expression and roles of proteins encoded by CircRNAs in tumorigenesis and development,this pa-per is expected to provide new tumor markers and potential targets for tumor diagnosis and treatment.

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 .

Objective To explore the change of glyoxalase I in type 2 diabetic ocular muscles palsy (DOMP) and its associations with advanced oxidation protein products (AOPP) and oxidative stress. Methods 58 DOMP patients, 50 T2DM and 30 normal controls were enrolled in this study. Levels of blood lipids, fasting blood glucose, hemoglobin A1c, insulin, serum glyoxalase I, AOPP, malondialdehyde (MDA), superoxide dismutase (SOD) and total antioxidant capacity (T-AOC) were measured. Homeostasis model assessment was performed to evaluate the status of insulin resistance (IR). Results Levels of high-density lipoprotein cholesterol, SOD and T-AOC were positively correlated with glyoxalase I and inversely associated to AOPP. Levels of triglycerides , low-density lipoprotein cholesterol , fasting blood glucose , hemoglobin A1c , IR and MDA were negatively correlated with glyoxalase I and positively related to AOPP. AOPP had an inverse association with glyoxalase I (r = -0.823, P < 0.001). Multivariate regression analysis showed that serum levels of glyoxalase I (Sβ = 0.554) and AOPP (Sβ= -0.469) were influencing factors of groups. Conclusion Serum glyoxalase I levels were significantly decreased in DOMP and correlated with AOPP and levels of oxidative stress , which suggest that glyoxalase I could play crucial roles on the development of DOMP.

Objective To investigate the effect and mechanism of RNAi-mediated STAT3 gene silencing on epithelial-to-mesenchymal transition (EMT) of human pancreatic cancer cells.Methods Lentivirus vector mediating RNA interference targeting STAT3 was constructed in SW1990 cell line.The invasion ability of SW1990 cells was determined by cell invasion assay in vitro.Cell proliferation and cell cycle of SW1990 cells were also detected.The expression of EMT related genes such as STAT3,P-STAT3,Twist,Snail and E-cadherin were analyzed by reverse transcription-PCR,real-time PCR,and Western blotting.Results Silencing of STAT3 with RNAi not only markedly reduced proliferation but also greatly decreased the invasion ability of SW1990 cells.The mRNA level and protein expression of Snail decreased significantly (P ＜ 0.05),but those of E-cadherin increased significantly (P ＜ 0.05),compared to parental cells.However,no difference was on the expression of Twist in SW1990 cell line.Conclusions STAT3 signaling pathway plays an important role in the process of EMT.Silencing of STAT3 with RNAi can significantly inhibit EMT by downregulating expression of Snail and E-cadherin in pancreatic cancer cells.

Objective To study the relationship between the expression of Caveolin-1 (Cav-1) and epithelial-mesenchymal transition(EMT) or metastasis in human pancreatic cancer.Methods The Cav-1 protein and EMT markers in highly metastatic pancreatic cancer cell lines (L3.7,Panc02-H7) and poorly metastatic pancreatic cancer cell lines (COLO357,Panc02) was detected by Western blotting and immunofluorescence.The morphology of the pancreatic cancer cells were observed under phase-contrast photomicrographs.The plasmids pcDNA3.1-caveolin-1 and control vector pcDNA3.1 were transfected into COLO357 cells by Lipofectamine LTX.The expression of Cav-1 protein,E-cadherin and vimentin were detected,and the morphology of COLO357 cells observed.Results L3.7 and Panc02-H7 cells had strong positive Cav-1 staining and high expression of mesenchymal marker (vimentin,N-cadherin) and low epithelial marker (E-cadherin,β-catenin),whereas COLO357 and Panc02 cells with typical epithelial morphology were weak positive in Cav-1 staining and of low expression of vimentin,N-cadherin and high expression of E-cadherin,β-catenin.In Cav-1 transfected COLO357 cells vimentin expression increased,and E-cadherins decreased resulting in typical morphology changes of EMT.Conclusions Overexpression of caveolin-1 is correlated with epithelial-mesenchymal transition of pancreatic cancer cells and cancer metastasis.

Objective To investigate the effects and mechanism of IL-6 on the epithelial to mesenchymal transition of human pancreatic cancer cells.Methods IL-6 was added into the culture media of human pancreatic cancer cells Capan-2,SW1990,and STAT3-siRNA-SW1990.Cell growth was measured by MTT assays.STAT3,p-STAT3,Snail,Twist,and E-cadherin mRNA and protein expression were examined using real-time fluorescence quantitative polymerase chain reaction (RT-PCR)and Western blot,respectively.The invasion abilities of SW1990 and Capan-2 cells were determined by a cell invasion assay in vitro.Results Our results showed that 100 μg/L of IL-6 significantly promoted the growth and invasion abilities of Capan-2 and SW1990 cells (P＜0.05).The use of IL-6 not only markedly increased the protein expression of P-STAT3 and Snail,but also greatly decreased the mRNA and protein expression of E-cadherin.The use of IL-6 can not change the mRNA and protein expression of Snail and E-cadherin.Conclusion Activation of the STAT3 signal transducer pathway with IL-6 can promote the epithelial to mesenchymal transition of pancreatic cancer cells in vitro through up-regulation of Snail and down-regulation of E-cadherin expression.Therefore the STAT3 signal transducer may provide a novel therapeutic target for the treatment of pancreatic cancer.

Objective To screen the genes related with signal transducers and activators of transcription 3 (STAT3) regulating pancreatic cancer invasion and metastasis by gene chips.Methods Human pancreatic cancer cell line SW1990 stably expressing low level of Stat3 was established by lentivirus transfection,while cells transfected with mock plasmid and cells without transfection served as control groups.The differences of invasion and metastasis related genes expression among the three groups were screened by gene chips.STAT3 mRNA and protein expression was measured by real-time PCR and Western blot.Three differentially expressed genes (MMP-7,IL-1β and IgTα7) were verified.ResultsThe expression level of STAT3 mRNA was 0.391 ± 0.037 after pancreatic cancer SW1990 cell trarsfected with STAT3 targeted lentivirus,which was significantly lower than those in mock plasmid group (1.002 ± 0.015) and nontransfected group ( 1.206 ± 0.042,P ＜ 0.05 ) ; the expression level of STAT3 protein was 182.38 ± 65.32,which was significantly lower than those in mock plasmid group (223.40 ±58.40) and non-transfected group (212.33 ±53.69).Eight invasion and metastasis related genes of SW1990 lowly expressing Stat3 were upregulated,while 3 genes were down-regulated.By verification,the mRNA level of MMP-7 and IL-1β were lower than in control group transfected with mook plassmid(0.287 ± 0.115 vs 1.010 ± 0.124,t =19.45,P =0.000;0.490 ± 0.10 vs 1.002 ± 0.002,t =13.83,P =0.000),but the mRNA level of IgTα7 was not decreased (1.173 ±0.280 vs 0.998 ±0.003,t =4.236,P =0.094).Meanwhile,the protein level of MMP-7 was significantly down-regulated when Stat3 was knocked down.ConclusionsStat3 causes changes of expressions of many invasion and metastasis-related genes of SW1990,and MMP-7 may be the main target gene regulated by Stat3.

ObjectiveTo evaluate the clinical efficiency and safety of cefmetazon in the prevention Department of General Surgery,First People's Hospital,Shanghai Jiaotong University,Shanghai 200080,Chinaand or treatment of infections in general surgery. MethodsA multicenter,prospective and open-labeled trial was conducted. In the prevention group,1700 patients were enrolled in clean-infection surgery,cefmetazon was given 1 g iv half an hour before the surgery started,and 1 g iv twice daily after the surgery for 3 days.Clinical response was evaluated in terms of both cure ( disappearance of pre treatment symptoms)and pathogen. In the treatment group,897 patients were diagnosed as peritonitis, cholecystitis and cholangitis,the patients were given cefmetazon 2 g iv twice a day for 7 - 14 days,clinical response and microbiological efficacy were assessed.ResultsIn prophylactic group,1449 patients were finally included.The clinical efficacy was 100％ (1449/1449).In the treatment group,a total of 897 patients were enrolled,and 110 patients failed for assessment of clinical efficacy,787 patients were included in the PPS population,the clinical efficacy was 90.7％ (714/787); Bacterial eradication rate was 92％ (46/50).Adverse reaction rates in prevention group and treatment group were 1.3％ (22/1700) and 1.2％ (11/897),including mild nausea and vomitting.ConclusionsCefmetazon is effective and safe in prevention and treatment of Postoperative infections in general surgery.

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.

Stat3 is a member of the STAT (signal transducer and activator of transcription) protein family. It can be activated by many cytokines, growth factors and carcinogens. Activation of Stat3 in the cytoplasm leads to its dimerization, translocation into the nucleus, DNA binding and gene transcription. Constitutively activated Stat3 is associated with cellular transformation, invasion, metastasis, angiogenesis, chemoresistance and radioresistance, and therefore suppress apoptosis of cancer.