论文部分内容阅读
本研究旨在观察地高辛对人胃癌MKN45细胞迁移和侵袭能力的影响,并探讨其分子机制。取人胃癌MKN45细胞作为研究对象,采用Transwell法检测细胞迁移和侵袭能力,通过脂质体转染法将星形细胞上调基因-1(astrocyte elevated gene-1,AEG-1)sh RNA干扰质粒转染MKN45细胞以构建低表达AEG-1的细胞株,利用Western blot法检测基质金属蛋白酶-9(matrix metalloproteinase-9,MMP-9)、E-钙粘蛋白(E-cadherin)和AEG-1等蛋白的表达变化。结果显示,地高辛可使MKN45细胞迁移率和侵袭率均显著下降(P<0.05),下调MMP-9和AEG-1蛋白表达水平(P<0.05)以及上调E-cadherin蛋白表达水平(P<0.05),上述作用均具有剂量依赖性。经sh RNA干扰AEG-1基因表达后,MKN45细胞中AEG-1蛋白表达水平显著下降(P<0.05);同时AEG-1干扰组MKN45细胞中E-cadherin蛋白表达水平显著升高(P<0.05),细胞迁移率、侵袭率和MMP-9蛋白表达水平均显著下降(P<0.05)。上述结果提示,地高辛可在体外剂量依赖性地抑制人胃癌MKN45细胞迁移和侵袭,这可能与地高辛抑制AEG-1蛋白表达,继而下调MMP-9蛋白表达和上调E-cadherin蛋白表达有关。
The aim of this study was to investigate the effects of digoxin on the migration and invasion of human gastric cancer MKN45 cells and its molecular mechanism. The human gastric cancer MKN45 cells were taken as the research object, and the cell migration and invasion ability were detected by Transwell method. The astrocyte elevated gene-1 (AEG-1) sh RNA interference plasmid transfection Staining of MKN45 cells to construct a cell line with low expression of AEG-1, Western blot was used to detect the expression of matrix metalloproteinase-9 (MMP-9), E-cadherin and AEG-1 Changes in protein expression. The results showed that digoxin can significantly reduce the migration and invasion of MKN45 cells (P <0.05), down-regulate the expression of MMP-9 and AEG-1 protein (P <0.05) and upregulate the expression of E-cadherin protein <0.05), the above effects are dose-dependent. The expression of AEG-1 protein in MKN45 cells was significantly decreased by sh RNA interference (P <0.05), while the expression of E-cadherin protein in MKN45 cells was significantly increased by AEG-1 interference (P <0.05 ), Cell migration rate, invasion rate and MMP-9 protein expression were significantly decreased (P <0.05). These results suggest that digoxin may inhibit the migration and invasion of human gastric cancer MKN45 cells in a dose-dependent manner in a dose-dependent manner, which may be related to digoxin inhibiting AEG-1 protein expression, then down-regulating MMP-9 protein expression and up-regulating E-cadherin protein expression related.