The role of long noncoding RNAs (lncRNAs) in the epithelial‐mesenchymal transition (EMT) in pancreatic ductal adenocarcinoma (PDAC) is unclear. Some lncRNAs can be transferred by extracellular vesicles (EVs) and have potential as biomarkers. Here, we identify an lncRNA that could serve as a biomarker for PDAC and show the functional roles of the lncRNA. Expression profiling of lncRNAs revealed that highly upregulated in liver cancer (HULC) was highly expressed, and induced, by transforming growth factor‐β in PDAC cells and their EVs. Knockdown of HULC decreased PDAC cell invasion and migration by inhibiting the EMT. Thus, HULC could be transferred by EVs, and promote EMT, invasion, and migration in recipient PDAC cells. To assess the roles of HULC, PDAC cell xenografts in nude mice were established. Knockdown of HULC in PDAC cells implanted in mice inhibited tumor growth. Moreover, microRNA‐133b suppressed PDAC cell invasion and migration by inhibiting the EMT through targeting HULC. Furthermore, serum samples were obtained from 20 PDAC and 22 intraductal papillary mucinous neoplasm (IPMN) patients, as well as 21 healthy individuals. Analysis of serum EV HULC expression by digital PCR showed that HULC expression was significantly increased in PDAC patients compared to healthy individuals or IPMN patients. Additionally, HULC showed good predictive performance for discriminating PDAC, suggesting that the analysis of EV‐encapsulated HULC would contribute to the diagnosis for human PDAC. Extracellular vesicle‐transported HULC promotes cell invasion and migration by inducing the EMT, and microRNA‐133b suppresses the EMT by targeting HULC. Extracellular vesicle‐encapsulated HULC could be a potential circulating biomarker for human PDAC.

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Although it has been shown that bile acids possess antibacterial activity against Helicobacter pylori, few reports on their activity have been published. We determined the minimum inhibitory concentration at 72 h of various unconjugated and conjugated bile acids against laboratory standard strains and clinical isolates of H. pylori, and studied morphologic changes of H. pylori under the scanning electron microscope during treatment with deoxycholic acid and ursodeoxycholic acid at the minimum inhibitory concentrations for 24 h. We found that only the unconjugated form of dihydroxy bile acid has antibacterial activity. The minimum inhibitory concentration of deoxycholic acid is 200-400 microg/ml, that of chenodeoxycholic acid is similar to that of deoxycholic acid, and that of ursodeoxycholic acid is 400-800 microg/ml. The morphology of H. pylori changed from its primary rodlike shape to a spherical shape with blebs on the cell surface, and was further degraded to an irregularly condensed mass, following an increase in bile acid. This morphologic change in H. pylori was different from the change to a spherical shape caused by amoxicillin. On the basis of these results, it seems that unconjugated dihydroxy bile acid might be a candidate drug for eradication of H. pylori, but further investigations of the clinical usefulness of bile acid for this purpose should be done.

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