ABSTRACT
Objective To investigate the expression of LncRNA LINC00857 in pancreatic cells and the effect of lncRNA LINC00857 down-regulation on proliferation, migration and apoptosis of pancreatic cancer PANC-1 cells and possible mechanism. Methods The lentiviral vector GV112 was constructed and infected PANC-1 cells to obtain experimental group, while the blank plasmid was transfected as a negative control group and the cells without intervention were taken as normal control group. CCK-8 assay, Transwell assay, scratch test, flow cytometry, Western blot were used to detect the effect of LINC00857 down-regulation on cell proliferation, migration, apoptosis, cell cycle and EMT-related proteins. Results LINC00857 expression in pancreatic cancer cells were significantly higher than that in normal pancreatic epithelial cells (P < 0.001). Knockdown of LINC00857 could significantly inhibit the proliferation and migration of PANC-1 cells (P < 0.0001); compared with the negative control group, the apoptosis rates of cells in the experimental groups were significantly increased (P < 0.05), the number of cells in G0/G1 phase increased (P < 0.01), the number of cells in S phase decreased (P < 0.05), and the cells were blocked in the G1 phase, E-cadherin expression was significantly up-regulated (P < 0.05) and N-cadherin and Vimentin expression were significantly down-regulated (N-cadherin: P < 0.01, Vimentin: P < 0.05). Conclusion LINC00857 can promote proliferation and migration of PANC-1 cells and inhibit its apoptosis by regulating G1/S phase transition and EMT signaling pathway.
ABSTRACT
@#Alzheimer''s disease (AD) is the most common cause of senile dementia, accounting for an estimated 60% to 80% of cases, but there are no approved drugs to slow or stop the progressive clinical decline in the past years.Amyloid cascade hypothesis is recognized as the major etiologic basis for AD, however, the failures of several amyloid plaque-targeted programs have led many to dismiss the amyloid beta (Aβ) hypothesis of AD. Several reports show that soluble oligomers of Aβ (AβOs), which appear in brains more than 10 years before the clinical syndrome, are more toxic than Aβ plaque, causing synaptic dysfunction and neuronal apoptosis. Some agents that can effectively inhibit Aβ oligomer formation or block their toxicity made significant efficacy in clinical 2 and 3 trials, with the potential to be approved for the treatment of AD. This article reviews the recent development of AD drugs targeting Aβ oligomers, analyzes their structural characteristics, mechanism of action, preclinical and clinical data, and discusses the future direction of AD treatment, thus providing new strategies for AD drug research.