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Hepatocellular carcinoma (HCC) is one of the most common cancers worldwide. Its invasiveness and ability to metastasize contributes to an extremely high patient mortality. However, the molecular mechanisms that underlie the characteristics of HCC progression are not well understood. BRF2 has been shown to be an oncogene in a number of tumors; however, its role in HCC has not yet been thoroughly examined. In this study, we identified and validated BRF2 as an oncogene in HCC, providing a new insight into HCC pathogenesis and therapeutic possibilities. We showed that BRF2 expression was significantly upregulated in HCC cell lines and tissues, while BRF2 depletion suppressed HCC metastasis and invasion. We then examined the upstream regulation of BRF2 and identified miR-409-3p as being predicted to bind to the 3′ UTR of BRF2. We used a luciferase activity assay and functional verification to show that BRF2 is downregulated by miR-409-3p. Finally, we used bioinformatic analysis to show that BRF2 may be related to early HCC development through the Wnt/β-catenin signaling pathway.

Aim: To investigate whether bile survivin and carbohydrate antigen 199 (CA199) can be helpful in distinguishing cholangiocarcinoma (malignant obstructive jaundice) from benign obstructive jaundice. Methods: Receiver operating characteristic curve was used to evaluate the feasibility of bile survivin and CA199 in differentiating cholangiocarcinoma from benign obstructive jaundice. Results: The area under the curve for survivin and CA199 in bile and serum were 0.780 (p < 0.001), 0.6 (p = 0.084), 0.746 (p < 0.001) and 0.542 (p = 0.464), respectively. Combination of bile survivin and CA199 could improve the diagnostic capability. Conclusion: Bile survivin and CA199 are significantly increased in patients with cholangiocarcinoma and may be useful biomarkers in differentiating distinguishing cholangiocarcinoma from benign obstructive jaundice.

Chemoresistance of colon cancer cells to the chemotherapeutics is still a main obstacle in treatment of this malignancy. The microRNA (miRNA) mediated chemosensitivity regulation in colon cancer cells is still largely unknown. Here we constructed a fluorouracil (5-Fu) resistant SW480 cell line (SW480/5-Fu) and discovered that miRNA miR-494 was down-regulated in the drug resistant cells compared with the parental cells. miR-494 level was found to be correlated with 5-Fu sensitivity in colon cancer cells, and artificial alteration of miR-494 affects the sensitivity of colon cancer cell lines to 5-Fu. miR-494 also promoted apoptosis of colon cancer cells at present of 5-Fu. Importantly, as a regulatory enzyme in the 5-Fu catabolic pathway, DPYD was confirmed to be a direct target of miR-494 through the interaction of miR-494 and its binding site within DPYD 3' untranslated region (3'UTR). miR-494 also negatively regulated endogenous DPYD expression in SW480 cells. Overexpression or knockdown of DPYD could attenuate miR-494 mediated 5-Fu sensitivity regulation, suggesting the dependence of DPYD regulation in miR-494 activity. miR-494 inhibited SW480/5-Fu derived xenograft tumors growth in vivo at present of 5-Fu. Thus, we concluded that in colon cancer cells, tumor suppressor miR-494 enhanced 5-Fu sensitivity via regulation of DPYD expression.

This study aimed to identify the effect of percutaneous transhepatic biliary drainage (PTBD) combined with 3-dimensional conformal radiotherapy (3D-CRT) in comparison with PTBD therapy only on the treatment of unresectable Klatskin tumors (KTs).Thirty-seven patients with unresectable KTs were included in the study. Twenty-six patients received PTBD and 3D-CRT successively, whereas the other 11 patients received PTBD only. Changes in the clinical symptoms after the PTBD treatment, the radiotherapy effect, and the survival time were recorded and analyzed.The clinical symptoms of the 2 groups gradually decreased after the PTBD treatment. The radiotherapy effect showed an overall effective rate (complete response+partial response) of 17 (65.38%), and the serum carbohydrate antigen-19-9 levels before and after 3D-CRT were significantly different (P0.001). The mean survival time of the PTBD group was 11.27 months; the 1- and 2-year cumulative survival rates were 36.4% and 9.1%, respectively. The mean survival time of the combined therapy group was 22.77 months; the 1-, 2-, and 3-year cumulative survival rates were 53.8%, 38.5%, and 11.5%, respectively. The log-rank test showed that the patients who received combined therapy had longer survival time than the patients who only received PTBD (P=0.001).Patients with unresectable KTs who underwent PTBD could relieve biliary obstruction effectively. Although this study is not a randomized trial, 3D-CRT combined with PTBD seems to be a promising and an effective method as a palliative treatment for unresectable KTs.

Norcantharidin (NCTD) is an efficacious anti-cancer drug that has been used in China for many years, but its underlying mechanism of action is still not fully understood. In the present study, we found that NCTD could induce morphological changes in colon cancer cells, causing a transition from a spindle-shaped morphology to a typical round or oval shape, which was indicative of a mesenchymal-epithelial transition (MET) process. Next, we investigated the mechanism by which NCTD induced the MET process. Using a transwell assay, we found that NCTD could suppress the migratory and invasive ability of colon cancer cells in a dose-dependent manner. Moreover, NCTD suppressed the expression of integrin αvβ6, MMP-3 and MMP-9 as well as the polymerization of F-actin, further supporting its suppressive effect on migratory and invasive ability. Furthermore, the expression of αvβ6, N-cadherin, vimentin and phosphorylated ERK was decreased, while the expression of E-cadherin was up-regulated. We verified that phosphorylated Ets1 was down-regulated substantially after treatment with NCTD. Taken together, our data demonstrated that NCTD could inhibit the EMT process of colon cancer cells by inhibiting the αvβ6-ERK-Ets1 signaling pathway. This study revealed part of the mechanism through which NCTD could reverse the EMT process in colon cancer.

Todani classification is extensively used to guide the surgical strategy of choledochal cysts, but no systematic investigations on the distal management of intrapancreatic choledochal cysts have been conducted. This study reports the distal classification and management of choledochal cysts in adults based on the relation between the cyst and pancreatic duct. Patients with choledochal cyst who underwent operation, including distal management, in our department from January 2009 to December 2014 were retrospectively reviewed. Patients presenting symptoms, coexisting diseases, surgical treatment, perioperative complications, and long-term follow-up according to the distal classification of choledochal cyst were analyzed. A total of 54 patients with choledochal cyst were included in the present retrospective study. Based on the distal classification of choledochal cyst, 39 patients (72.22%) were type 1, 13 patients (24.07%) were type 2, and 2 patients (3.70%) were type 3. Thirty-nine type 1 patients and 10 type 2 patients underwent excision of intrapancreatic choledochal cyst or bile duct. Three type 2 patients received excision of distal cylindrical cyst and papilla, followed by pancreatic duct plasty with duodenum mucosa. One type 3 patient underwent endoscopic sphincteroplasty, and another type 3 patient underwent transduodenal sphincteroplasty. After the operation, 11 patients (20.37%, 11/54) had short-term perioperative complications. The long-term follow-up results showed that the satisfactory rate (excellent and good outcomes) was 95.83%. Current distal classification of choledochal cysts could provide a more targeted strategy for complete excision to eliminate potential dead space within the pancreas, protect the pancreatic duct, and prevent reoperation.

Chemoresistance of colon cancer cells to the chemotherapeutics is still a main obstacle in treatment of this malignancy. The microRNA (miRNA) mediated chemosensitivity regulation in colon cancer cells is still largely unknown. Here we constructed a fluorouracil (5-Fu) resistant SW480 cell line (SW480/5-Fu) and discovered that miRNA miR-494 was down-regulated in the drug resistant cells compared with the parental cells. miR-494 level was found to be correlated with 5-Fu sensitivity in colon cancer cells, and artificial alteration of miR-494 affects the sensitivity of colon cancer cell lines to 5-Fu. miR-494 also promoted apoptosis of colon cancer cells at present of 5-Fu. Importantly, as a regulatory enzyme in the 5-Fu catabolic pathway, DPYD was confirmed to be a direct target of miR-494 through the interaction of miR-494 and its binding site within DPYD 3' untranslated region (3'UTR). miR-494 also negatively regulated endogenous DPYD expression in SW480 cells. Overexpression or knockdown of DPYD could attenuate miR-494 mediated 5-Fu sensitivity regulation, suggesting the dependence of DPYD regulation in miR-494 activity. miR-494 inhibited SW480/5-Fu derived xenograft tumors growth in vivo at present of 5-Fu. Thus, we concluded that in colon cancer cells, tumor suppressor miR-494 enhanced 5-Fu sensitivity via regulation of DPYD expression.

Aim: Increased expression of High Mobility Group Protein Box 1(HMGB1) has been reported with several different tumor types, but the role of HMGB1 in pancreatic cancer is not fully understood. The aim of this study is to detect the expression of HMGB1 and evaluate the role of HMGB1 in pancreatic cancer. Methods: The expression level of HMGB1 in pancreatic cancer cell line PANC-1 was detected by western blot analysis and reverse transcription PCR. Furthermore, primary tumors tissues of 35 patients with resected pancreatic cancer(T2-4 N0-2 M0-1) were stained immune histochemically using the polyclonal anti-HMGB1 antibody. The prognostic relevance of HMGB1 expression was evaluated by univariate Kaplan-Meier among 35 patients. Results: HMGB1 is over expressed in pancreatic cancer.HMGB1 overexpression was significantly associated with clinical stage (p

The intrusion detection under the environment of IPv6 is an important security technology along with firewall in system security defense system, which can be used for real-time detection and monitoring of the system in the whole process of system invasion. This paper puts forward an intrusion detection system under IPv6 platform based on intrusion detection feature attribute reduction by using pattern matching, so as to expand the range of application and user group of the security products. By the analysis and comparison of various pattern matching algorithms, the new algorithm realizes the intrusion feature module matching under IPv6, and make detection system be of high efficiency. Later experiments have proved this view.

This paper reviews the network distance education teaching mode, Using the computer education as an example, the analysis of the computer aided teaching method the results in the application of quantitative and qualitative analysis method. Make a certain university 2005 freshmen do level test, according to the principle of no significant difference will be divided into a whole new N. Randomly selected two whole (62) for the test group to participate in university computer teaching reform. At the same time, select the other two whole (62) as the reference object for regular teaching. Period, and the two groups of students in four tests, and the four scores on the quantitative analysis; The network distance education in computer aided teaching experience of teachers and students class separately carried on the interview, At the same time, to student's online autonomous learning time and content monitoring and statistics, and student test scores were compared.