ObjectiveOur study aimed to investigate the interaction between peroxiredoxin 1 (Prx1) and forkhead box O3 (FOXO3) and to explore the role of PI3K/AKT pathway in the development of pancreatic cancer.Material and methodsHuman pancreatic normal cells HPDE6-C7 and pancreatic cancer cells PANC-1 were randomly divided into control group, Prx1-silencing (si-Prx1) group, Prx1/FOXO3 dual-silencing (si-Prx1/FOXO3) group, and negative control group. Cell proliferation assay, clone formation assay, and cell apoptosis assay were performed to investigate the effects of Prx1 silencing and FOXO3 silencing on the proliferation and apoptosis ability of pancreatic cancer cells. qRT-PCR and Western blot were performed to study the Prx1 and FOXO3 mRNA in the two cells and FOXO3 protein expression in PANC-1 cells.ResultWe found Prx1 silencing could inhibit growth and promote apoptosis of PANC-1 cells. And Prx1 silencing could decrease the Prx1 mRNA level and increase FOXO3 mRNA level. To further explore the role of Prx1 in PI3K/AKT, we study the cell proliferation and apoptosis ability after adding the PI3K inhibitor and PI3K activator. We observed that PI3K inhibitor could inhibit tumor cell growth and promote cell apoptosis. And PI3K inhibitor also downregulated Prx1 protein expression.ConclusionWe concluded that the Prx1 silencing inhibited the growth and promoted apoptosis of pancreatic cancer cells via modulation of PI3K/AKT pathway by targeting FOXO3 gene.
The aim of this study was to explore the mechanism of racemic higenamine in the treatment of sick sinus syndrome (SSS). A total of 40 New Zealand rabbits were randomly divided into normal sinus node and damaged sinus node (SND) groups, and each group was randomly divided into treatment and control groups (n=10). The SND model was established by formaldehyde wet dressing of the sinus node area. The treatment groups were administered an intravenous infusion of 0.04 mg/kg racemic higenamine via the marginal ear vein within 5 min. The electrophysiological indicators of sinoatrial function, including the sinus node recovery time (SNRT), corrected sinus node recovery time (CSNRT), total sinoatrial conduction time (TSACT) and sinus cycle length (SCL), were determined before and 20 min after medication and the changes in these indicators were evaluated. The two control groups were administered 10 ml physiological saline. Following the administration of racemic higenamine, the SNRT, CSNRT, TSACT and SCL in the normal sinus node and SND groups were significantly shortened compared with those in the control groups (P<0.01). The electrophysiological influence of racemic higenamine on sinoatrial function in the SND group was significantly greater than that in the normal sinus node group (P<0.01), and its effect in the treatment of arrhythmia caused by a damaged sinus node was statistically significant (P<0.05). The main electrophysiological mechanism of racemic higenamine in the treatment of SSS was the enhancement of sinus node self-discipline and improvement of sinoatrial and atrioventricular conduction function.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.