ABSTRACT
AIM:To investigate the effects of peroxiredoxin 4 ( Prdx4) protein expression levels on the migra-tion and invasion of human cervical cancer HeLa cells.METHODS:The plasmid pcDNA3.0-HA-Prdx4 was transfected into HeLa cells.The HeLa cells were infected with LV-Prdx4 RNAi vector to establish stable Prdx4 shRNA HeLa cells. The change in the expression of Prdx4 protein was validated by Western blotting.The wound-healing assay, and Transwell migration and invasion assays were performed to detect the migration and invasion of HeLa cells, respectively.RESULTS:The expression of Prdx4 protein was up-regulated in the HeLa cells after transfection with pcDNA3.0-HA-Prdx4 plasmid ( P<0.05), whereas it was down-regulated in the Prdx4 shRNA HeLa cells (P<0.05).The abilities of migration and inva-sion were significantly increased in Prdx4-overexpressing HeLa cells compared with non-transfected and mock plasmid trans-fected control groups ( P<0.01) .When Prdx4 was knocked down by shRNA, the migration and invasion of the HeLa cells were remarkably repressed compared with blank control group and negative control group ( P<0.01 ) .CONCLUSION:The up-regulation of Prdx4 expression facilitates the migration and invasion of HeLa cells, and the down-regulation of Prdx4 expression inhibits the migration and invasion of HeLa cells, indicating that Prdx4 may be a potential molecular target for cervical cancer therapy.
ABSTRACT
Objective To investigate the relationship between expression of nuclear factor kappa B p65 ( NF-κB p65) and hippocampal neuronal apoptosis in acute necrotizing pancreatitis (ANP) rats with brain injury. Methods Sixty-four SD rats were randomized into normal saline group (NS) and ANP group. The ANP rat model was induced by retrograde injection of 4% sodium taurocholate into the pancreaticobiliary duct of SD rats. Nissle stain was used to detect the brain injury. Neuronal apoptosis was determined by TUNEL.NF-κB p65 expression was detected by immunohistochemistry and RT-PCR. Results Hippocampal neuron was absent, karyopyknosis, unclear nucleolus and decreased Nissl bodies were found, the injuries was aggravated with time. The apoptosis index at the 3, 6 and 12 h in ANP group was 10.63 ±0.24, 21.02±0.25, 17.12±0.36, respectively, while they were 0.33±0.19,0.71±0.67, 0.45 ± 0. 33 in NS group, and the difference was statistically significant ( P ＜ 0. 01 ). The expressions of NF-κB p65 mRNA were 0. 63 ± 0.05,1.05 ±0.06,0.92 ±0.05, which were significantly higher than those in the NS group (0.11 ±0.01,0.12±0.01,0.08±0.01,P＜0.05).The chatge of expression of NF±κB p65 protein was consistent with that of NF-κB p65 mRNA. Conclusions The brain injury of ANP rats was highly correlated with neuronal apoptosis at the early and middle phase of ANP, and its mechanism may be related with NF-κB p65 activation.