3-Hydroxy-3-methylglutaryl reductase degradation (HRD1) is an E3 ubiquitin ligase that functions by promoting degradation of misfolded proteins in processes such as embryogenesis and rheumatoid arthritis. However, little is known about the role of HRD1 in cancer. The aim of the present study was to investigate the expression pattern and functions of HRD1 in human colon cancer (CC). We found that HRD1 expression was increased significantly in human CC tissues, and its overexpression was associated with TNM stage, tumor differentiation, tumor invasive depth, and distant metastasis. Knockdown of HRD1 using small hairpin (sh) RNA plasmid significantly inhibited CC cell migration and invasion. Furthermore, the silencing of HRD1 decreased the expression of MMP-2 and MMP-9, which is critical for CC cell migration and invasion. Taken together, these results revealed that HRD1 is overexpressed in CC and promotes migration and invasion of CC cells. Inhibition of HRD1 may be considered as an effective anti-CC strategy.

BACKGROUND AND OBJECTIVE:Common bile duct (CBD) stones are common in patients even after cholecystectomy. Besides endoscopic retrograde cholangiography (ERCP), laparoscopic common bile duct exploration (LCBDE) is also applied. This study aims to compare clinical indications, therapeutic benefits and complications for these two managements.METHODS:From October 2012 to February 2015, 1072 consecutive patients were diagnosed as choledocholithiasis in our single hospital. Post-cholecystectomy patients who underwent ERCP or LCBDE were included. Clinical data were analyzed, such as success rate, complications, procedure duration, postoperative hospital stay, total cost and recurrence of ductal stones. Prior ERCP, previous biliary anatomic alteration surgeries and lost to follow up were the excluding criteria.RESULTS:141 patients were included according to the criteria, and 87 cases underwent ERCP and 54 cases underwent LCBDE. Age and sex distribution of patients were comparable between the two groups. The success rate for CBD stones clearance was 97.7% in the ERCP group, compared with 87.0% in the LCBDE group (p=0.03). The mean procedure duration was also significantly shorter in ERCP group (52.0±15.8 vs. 102.9±40.1 min; p<0.001). Postoperative hospital stay was similar (5.5±2.6 vs. 5.9±2.3 days; p=0.40). And no significant difference for postoperative complications (3.4% vs. 11.1%; p=0.15), total cost ($3787.1±1061.5 vs. $3983.54±1257.1, p=0.32), and the rate of bile duct stones recurrence (6.9% vs. 7.4%, p=1.00).CONCLUSIONS:For clearing CBD stones in patients after cholecystectomy, ERCP was more efficient and might be the first choice, while LCBDE might be beneficial for patients with large stones.

ObjectiveTo know the effect of age on survival outcome in operated and non-operated patients with colon cancer.MethodsFrom the Surveillance, Epidemiology, and End Results database, we identified 123,356 patients with colon cancer who were diagnosed between 1996 and 2005, grouped them as older or younger than 40 years and analyzed their 5-year cancer-specific survival (CSS) data, along with some risk factors, using Kaplan-Meier methods and multivariable Cox regression models.ResultsThe younger group had significantly higher pathological grades (P<0.001), more mucinous and signet-ring histology (P<0.001), advanced AJCC stage (P<0.001), and were more likely to undergo surgery (P<0.001). For surgically treated patients, age did not significantly affect 5-year CSS (younger: 66.7%; older: 67.3%; P = 0.86). Further analysis showed that age was an independent prognostic factor in stage I-IV disease (stage I: P = 0.001; P<0.001 for stages II-IV, in both uni- and multivariate analyses), but not for patients with unknown disease stage (P = 0.52). For non-surgically treated patients, age significantly affected 5-year CSS (younger: 16.2%; older: 12.9%; P<0.001) in univariate analysis; and was an independent prognostic factor (P<0.001) in multivariate analysis.ConclusionThe CSS rate for younger CC patients was at least as high as for older patients, although they presented with higher proportions of unfavorable factors and more advanced disease.

Derlin-1 is overexpressed in many types of solid tumors and plays an important role in cancer progression. However, the expression pattern and functions of Derlin-1 in human colon cancer are not fully understood. In the present study, we examined Derlin-1 expression in colon cancer cell lines and human tissues and investigated its role in colon cancer. We found that Derlin-1 expression was increased significantly in colon cancer tissues and its overexpression correlated with the tumor differentiation, Dukes stage, invasion, lymph node metastasis, distant metastasis, and poor overall survival. The silencing of Derlin-1 by shRNA led to the growth inhibition of colon cancer cells, which were associated with the promotion of apoptosis. Furthermore, Derlin-1 silencing significantly inhibited the activation of the PI3K/AKT signaling pathway. Taken together, our results showed that Derlin-1 is overexpressed in colon cancer and promotes proliferation of colon cancer cells. Derlin-1 may be a potential therapeutic target for the treatment of colon cancer.

There have been more than 10 years since endoscopy was used to treat the chronic pancreatitis , including endoscopic pancreatic sphincterotomy , dilatation of pancreatic duct , endoscopic pancreatic stent deployment , etc. Endoscopic management could relieve the pain caused by chronic pancreatitis effectively , and improve the pancreatic functions .In other words , it could substitute the surgical therapy to some extent .Most cases with chronic pancreatitis were accompanied with other diseases , such as pancreatic duct stones , stricture of common biliary duct , and pancreatic pseudocyst , which also caused these symptoms and interacted as both causes and effected with chronic pancreatitis .Considering the efficacy of treatment , complication incidence and quality of life of patients, we find that endoscopic management can be chosen as the first treatment method for chronic pancreatitis and its co -morbidities .

A recently invented duodenal-jejunal bypass sleeve (DJBS) implanted in the duodenum and proximal jejunum has exhibited good glycemic control in diabetes mellitus. However, the specific mechanism by which DJBS placement induces the remission of diabetes is not well known. Previous studies have indicated that changes in the pattern of gut hormone secretion may play a role. The aim of the present study was to explore the role of intestinal L cells and the production of glucagon-like peptide-1 (GLP-1) by these cells in DJBS implantation-induced glycemic control in diabetic rats. A DJBS was placed in the proximal small intestine of rats with diabetes induced by a high-fat diet and low-dose streptozotocin (STZ), and the effects of the DJBS on the remission of diabetes and the GLP-1 levels of plasma and intestinal tissues were investigated 12 weeks after DJBS placement. The number of intestinal GLP-1 positive cells was also counted. When the DJBS had been in place for 12 weeks, the plasma glucose level of the DJBS-implanted rats decreased significantly from 23.33±1.56 mmol/l prior to surgery to 7.70±0.84 mmol/l and the diabetes mellitus was relieved completely; however, diabetic control rats and diabetic rats subjected to sham surgery did not show any improvement. Parallel with the remission of diabetes, the plasma and distal ileum GLP-1 levels of rats in the DJBS implantation group were also higher than those of rats in the diabetic control and sham surgery groups. The number of GLP-1-positive cells in the distal ileum was also higher in the DJBS implantation group than in the diabetic control and sham surgery groups (31.0±2.6 vs. 23.5±4.4 vs. 23.0±3.2 respectively; P<0.01). DJBS implantation effectively led to the remission of diabetes in rats with diabetes induced by a high-fat diet and low-dose STZ when implanted for 12 weeks. The remission of diabetes may be associated with the increase in the number of L cells and elevation of GLP-1 levels induced by DJBS implantation.

内镜黏膜下剥离术(endoscopic submucosal dissection,ESD)是由日本内镜医师发明的用于早期胃肠道恶性病灶整块切除的一种微创技术.现在在世界范围内已广泛开展,ESD提高了较大的早期胃肠道肿瘤整块切除的成功率.新设备和新技术的应用使ESD得到了很大的改进,如今ESD切除范围已经从胃扩展到了消化道其他黏膜区域,如食管、十二指肠、结肠和直肠,而且对于直径超过2 cm的消化道表浅肿瘤,ESD明显优于内镜下黏膜切除术(EMR),有较高的根治率,减少复发的风险,并可更好的进行组织学评估,最近的报道显示ESD提高了胃肠道肿瘤的五年总体生存率.2006年起国内也开始应用ESD治疗下消化道病变.

Recently, more and more evidence are rapidly accumulating that long noncoding RNAs (lncRNAs) are involved in human tumorigenesis and misregulated in many cancers, including colon cancer. LncRNA could regulate essential pathways that contribute to tumor initiation and progression with their tissue specificity, which indicates that lncRNA would be valuable biomarkers and therapeutic targets. Colon cancer-associated transcript 1 (CCAT1) is a 2628 nucleotide-lncRNA and located in the vicinity of a well-known transcription factor c-Myc. CCAT1 has been found to be upregulated in many cancers, including gastric carcinoma and colonic adenoma-carcinoma. However, its roles in colon cancer are still not well documented and need to be investigated. In this study, we aim to investigate the prognostic value and biological function of CCAT1 and discover which factors may contribute to the deregulation of CCAT1 in colon cancer. Our results revealed that CCAT1 was significantly overexpressed in colon cancer tissues when compared with normal tissues, and its increased expression was correlated with patients’ clinical stage, lymph nodes metastasis, and survival time after surgery. Moreover, c-Myc could promote CCAT1 transcription by directly binding to its promoter region, and upregulation of CCAT1 expression in colon cancer cells promoted cell proliferation and invasion. These data suggest that c-Myc-activated lncRNA CCAT1 expression contribute to colon cancer tumorigenesis and the metastatic process and could predict the clinical outcome of colon cancer and be a potential target for lncRNA direct therapy.

Data derived from massive cloning and traditional sequencing methods have revealed that long non-coding RNAs (lncRNA) play important roles in the development and progression of cancer. Although many studies suggest that the lncRNAs have different cellular functions, many of them are not yet to be identified and characterized for the mechanism of their functions. To address this question, we assay the expression level of lncRNAs-Loc554202 in breast cancer tissues and find that Loc554202 is significantly increased compared with normal control, and associated with advanced pathologic stage and tumor size. Moreover, knockdown of Loc554202 decreased breast cancer cell proliferation, induced apoptosis and inhibits migration/invasion in vitro and impeded tumorigenesis in vivo. These data suggest an important role of Loc554202 in breast tumorigenesis.