Background: Accumulating evidence indicates that circRNAs may serve as essential regulators in the progression of several human cancers, but the function and mechanism of circRNAs in intrahepatic cholangiocarcinoma (ICC) are largely unknown.
Methods: RNA-seq was used to assess differentially expressed circRNAs between 4 ICC and peritumor tissues. Quantitative RT-PCR and in situ hybridization were used to determine the circHMGCS1-016 expression in ICC tissues.
The overexpression or abnormal activation of cyclo‑oxygenase‑2 (COX‑2) has been reported in pancreatic cancer cells. NS‑398, a selective inhibitor of COX‑2, is unable to inhibit pancreatic cancer cell proliferation, as determined by a Cell Counting Kit 8 assay. However, it does increase cancer cell invasiveness, and therefore the invasiveness of the PANC‑1 cells was determined, along with the activation of P38, which was assessed by western blotting.
View Article and Find Full Text PDFIt is important to identify the severity of acute pancreatitis (AP) in the early course of the disease. Clinical scoring systems may be helpful to predict the prognosis of patients with early AP; however, few analysts have forecast the accuracy of scoring systems for the prognosis in hyperlipidemic acute pancreatitis (HLAP). The purpose of this study was to summarize the clinical characteristics of HLAP and compare the accuracy of conventional scoring systems in predicting the prognosis of HLAP.
View Article and Find Full Text PDFObjective: Pancreatic acinar cell necrosis and subsequent inflammatory response aggravate acute pancreatitis (AP). Tetraspanin CD9 has been reported to mediate inflammatory signaling by regulating molecular organization at the cell surface. This study aimed to investigate the role of CD9 in caerulein-induced AP (CIP) in mice.
View Article and Find Full Text PDFRecent studies have shown that microRNAs, a class of small and noncoding RNA molecules, play crucial roles in the initiation and progression of pancreatic cancer. In the present study, the expression and roles of miR-191 were investigated. Through both gain-of function and loss-of function experiments, a pro-oncogenic function of miR-191 was demonstrated.
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