Laparoscopic necrosectomy and the placement of an intermittent irrigation and continuous suction drainage system for IPN is feasible, effective, and of minimal invasiveness. The late laparoscopic necrosectomy is relatively difficult.

MicroRNAs (miRNAs) are known to be involved in the development and progression of pancreatic cancer (PAC). The expression levels and roles of miR-1252-5p in PAC remain unclear. Quantitative real-time PCR and in situ hybridization were used to detect miR-1252-5p expression in PAC cells and human tissues. We studied the gain and loss of function of miR-1252-5p in the PAC cell lines in vitro and in vivo . The direct targets of miR-1252-5p were analyzed using public databases and a dual-luciferase reporter assay. Expression levels of miR-1252-5p are downregulated in PAC cell lines and tissue samples, and its expression is negatively associated with adverse clinical features and poor prognosis. In vitro and in vivo experiments show that miR-1252-5p overexpression inhibits the proliferation, migration, invasion, and epithelial-mesenchymal transition of PAC cells, and miR-1252-5p knockdown enhances these biological behaviors. MiR-1252-5p negatively regulates neural precursor cell expressed, developmentally downregulated 9 (NEDD9) by directly binding its 3'- untranslated region. Further mechanism research revealed that the SRC/STAT3 pathway is involved in miR-1252-5p/NEDD9 mediation of PAC's biological behaviors. We also verified that Myb inhibited miR-1252-5p by directly binding at its promoter. MiR-1252-5p may act as a tumor-suppressing miRNA in PAC and may be a potential therapeutic target for PAC patients.

Background: Recurrence and metastasis are the major causes of pancreatic ductal adenocarcinoma (PDAC) mortality after treatment. The underlying molecular mechanism is poorly understood. Actin-related protein 3 (ACTR3) is an important component of the actin-related protein 2/3 complex, which is involved in the regulation of cell motility and epithelial mesenchymal transition (EMT) process. Previously published studies have indicated that ACTR3 expression is upregulated in several types of cancers, and promotes tumor development, including gastric cancer and hepatocellular carcinoma. However, to date, the expression levels and the role of ACTR3 in PDAC are not well understood.Methods: In the present study, the expression levels of ACTR3 in PDAC tissue and the relationship of ACTR3 expression with clinical prognosis were analyzed by mRNA microarray and bioinformatics. The biological functions and underlying mechanism of ACTR3 in PDAC were examined by a series of assays, including Cell Counting Kit-8 (CCK-8), transwell assay, and Western blotting.Results: We found that the expression of ACTR3 was significantly increased in PDAC tissues and cell lines. A higher expression of ACTR3 was predictive of poor outcome for patients with PDAC. In vitro, the knockdown of ACTR3 expression significantly inhibited the invasive and migratory capacity of PDAC cells, and altered the distribution of F-actin and the expression of EMT markers. Conclusions:The findings of our study indicated that ACTR3 promotes cell migration and invasion by inducing EMT in PDAC, which may be a potential therapeutic target and prognostic indicator for PDAC patients.