Clinical comparison of laparoscopy vs open surgery in a radical operation for rectal cancer: A retrospective casecontrol study

AIM: To assess the diverse immediate and longterm clinical outcomes, a retrospective comparison between laparoscopic and conventional operation was performed.METHODS: A total number of 916 clinical cases, from January 2006 to December 2013 in our hospital, were analyzed which covered 492 patients underwent the laparoscopy in radical resection(LRR) and 424 cases in open radical resection(ORR). A retrospective analysis was proceeded by comparing the general information, surgery performance, pathologic data, postoperative recovery and complications as well as long-term survival to investigate the diversity of immediate and long-term clinical outcomes of laparoscopic radical operation.RESULTS: There were no statistically significance differences between gender, age, height, weight, body mass index(BMI), tumor loci, tumor node metastasis stages, cell differentiation degree or American Society of Anesthesiologists scores of the patients(P > 0.05). In contrast to the ORR group, the LRR group experienced less operating time(P < 0.001), a lower blood loss(P < 0.001), and had a 2.44% probability of conversion to open surgery. Postoperative bowel function recovered more quickly, analgesic usage and the average hospital stay(P < 0.001) were reduced after LRR. Lymph node dissection during LRR appeared to be slightly more than in ORR(P = 0.338). There were no obvious differences in the lengths and margins(P = 0.182). And the occurrence rate in the two groups was similar(P = 0.081). Overall survival rate of ORR and LRR for 1, 3 and 5 years were 94.0% and 93.6%(P = 0.534), 78.1% and 80.9%(P = 0.284) and 75.2% and 77.0%(P = 0.416), respectively.CONCLUSION: Laparoscopy as a radical operation for rectal cancer was safe, produced better immediate outcomes. Long-term survival of laparoscopy revealed that it was similar to the open operation.

Down-regulation of STAT3 expression by vector-based small interfering RNA inhibits pancreatic cancer growth

AIM:To evaluate the effect of RNA interference (RNAi) mediated silence of signal transduction and activation of transcription (STAT)3 on the growth of human pancreatic cancer cells both in vitro and in vivo.METHODS:STAT3 specific shRNA was used to silence the expression of STAT3 in pancreatic cancer cell line SW1990.The anti-growth effects of RNAi against STAT3 were studied in vitro and in experimental cancer xenografts in nude mice.The potential pathways involved in STAT3 signaling were detected using reverse transcription polymerase chain reaction and western blotting.RESULTS:The expression of the STAT3 was inhibited using RNAi in SW1990 cells.RNAi against STAT3 inhibited cell proliferation,induced cell apoptosis and significantly reduced the levels of CyclinD1 and Bcl-xL when compared with parental and control vector-transfected cells.In vivo experiments showed that RNAi against STAT3 inhibited the tumorigenicity of SW1990 cells and significantly suppressed tumor growth when it was directly injected into tumors.CONCLUSION:STAT3 signaling pathway plays an important role in the progression of pancreatic cancer,and silence of STAT3 gene using RNAi technique may be a novel therapeutic option for treatment of pancreatic cancer.

Basic Study Long non-coding RNA TP73-AS1 promotes pancreatic cancer growth and metastasis through miRNA-128-3p/GOLM1 axis

BACKGROUND Previous studies have suggested that long non-coding RNAs(lncRNA)TP73-AS1 is significantly upregulated in several cancers.However,the biological role and clinical significance of TP73-AS1 in pancreatic cancer(PC)remain unclear.AIM To investigate the role of TP73-AS1 in the growth and metastasis of PC.METHODS The expression of lncRNA TP73-AS1,miR-128-3p,and GOLM1 in PC tissues and cells was detected by quantitative real-time polymerase chain reaction.The bioinformatics prediction software ENCORI was used to predict the putative binding sites of miR-128-3p.The regulatory roles of TP73-AS1 and miR-128-3p in cell proliferation,migration,and invasion abilities were verified by Cell Counting Kit-8,wound-healing,and transwell assays,as well as flow cytometry and Western blot analysis.The interactions among TP73-AS1,miR-128-3p,and GOLM1 were explored by bioinformatics prediction,luciferase assay,and Western blot.RESULTS The expression of TP73-AS1 and miRNA-128-3p was dysregulated in PC tissues and cells.High TP73-AS1 expression was correlated with a poor prognosis.TP73-AS1 silencing inhibited PC cell proliferation,migration,and invasion in vitro as well as suppressed tumor growth in vivo.Mechanistically,TP73-AS1 was validated to promote PC progression through GOLM1 upregulation by competitively binding to miR-128-3p.CONCLUSION Our results demonstrated that TP73-AS1 promotes PC progression by regulating the miR-128-3p/GOLM1 axis,which might provide a potential treatment strategy for patients with PC.