ABSTRACT
AIM:To investigate the function of microRNA-125a-5p (miR-125a-5p) on epithelial-mesenchy-mal transition ( EMT) of breast cancer cells via GSK-3β/Snail signaling pathway. METHODS:The expression of miR-125a-5p in normal breast epithelial cells and breast cancer cells, as well as the transfection efficiency of miR-125a-5p plas-mid in MDA-MB-231 cells was detected by RT-qPCR. The chemotaxis ability and invasion ability were detected by chemo-taxis assay and Transwell invasion assay. The changes of EMT-related markers, the protein level of phosphorylated glycogen synthase kinase-3β (p-GSK-3β) and the nuclear translocation of Snail were determined by Western blot. RESULTS:The expression of miR-125a-5p in the breast cancer cells was significantly lower than that in the normal breast epithelial cells. The expression of miR-125a-5p was significantly higher in MDA-MB-231/miR-125a-5p cells than that in MDA-MB-231/NC cells. The ability of epithelial growth factor (EGF) at 10 μg/L to induce chemotaxis of MDA-MB-231 cells was the stron-gest. Compared with MDA-MB-231/NC group, stimulation of EGF decreased the invasion ability of MDA-MB-231/miR-125a-5p cells, and resulted in the increase in E-cadherin expression, while significantly decreased the protein levels of vi-mentin and p-GSK-3β. Meanwhile, the nuclear localization of Snail was significantly inhibited. The invasion capacity of MDA-MB-231/miR-125a-5p+GAB2 cells was significantly enhanced compared with MDA-MB-231/miR-125a-5p +Con cells, the expression of E-cadherin was decreased, and the protein levels of vimentin and p-GSK-3β were significantly in-creased, while the nuclear localization of Snail was promoted. CONCLUSION:miR-125a-5p suppresses EMT via GSK-3β/Snail signaling pathway, thus inhibiting the invasion ability of breast cancer cells.
ABSTRACT
<p><b>OBJECTIVE</b>To study the effect of oxymatrine (Oxy) on airway inflammation and the distribution of dendritic cells (DC) in lung and spleen tissues of asthmatic mice.</p><p><b>METHODS</b>Fifty BALB/c mice were assigned into five groups (n=10): an asthma model group, a dexamethasone (Dex) treatment group and three Oxy treatment groups (Oxy dose: 20, 40 and 80 mg/kg respectively). The histological changes of lung tissues were observed by hematoxylin and eosin staining. The expression of 33D1 antigen (a marker of DC) in lung and spleen tissues were detected by immunohistochemical staining.</p><p><b>RESULTS</b>The inflammatory reactions of the lung tissues in the Dex or Oxy treatment groups were less severe than those in the asthma model group. 33D1 antigen was remarkably expressed in the lung and spleen tissues of the asthma model group. After Dex treatment, the expression of 33D1 antigen in the lung and spleen tissues decreased significantly (P<0.01). 33D1 antigen expression in the lung tissues was significantly reduced in all of the three Oxy treatment groups in a dose-dependent manner compared with that in the asthma model group (P<0.01). The treatment with Oxy of 40 and 80 mg/kg decreased significantly the 33D1 antigen expression in the spleen tissues (P<0.01).</p><p><b>CONCLUSIONS</b>Oxy can alleviate airway inflammation and reduce the number of DC in lung and spleen tissues of asthma mice, which may be contributed to the mechanism of Oxy for treatment of asthma.</p>