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目的:探讨5,7二甲氧基黄酮(5,7-DMF)对胰腺癌细胞上皮-间充质转化的影响及分子机制。方法:用不同浓度DMF处理人胰腺癌Panc-1细胞,利用划痕法检测5,7-DMF干预后Panc-1细胞侵袭转移能力变化;用Western blot检测5,7-DMF干预后Fox M1蛋白表达情况;Fox M1si RNA转染人胰腺癌Panc-1细胞后,用Western blot进而检测EMT相关上皮标志分子E-cadherin、间质标志分子N-cadherin蛋白水平的表达变化。结果:5,7-DMF以浓度依赖方式显著抑制Panc-1细胞侵袭转移能力。5,7-DMF干预胰腺癌细胞后显著下调Fox M1表达水平;Fox M1 si RNA转染胰腺癌细胞,EMT相关分子E-cadherin表达升高,而N-cadherin表达降低,且与对照组相比均有统计学意义。结论:5,7二甲氧基黄酮可逆转胰腺癌细胞上皮-间充质转化,可能通过下调Fox M1水平是其重要机制之一,但其内在的分子机制尚需进一步探讨。
Objective: To investigate the effect of 5,7-dimethoxyflavone (5,7-DMF) on epithelial-mesenchymal transition of pancreatic cancer cells and its molecular mechanism. Methods: Human pancreatic cancer Panc-1 cells were treated with different concentrations of DMF. The invasion and metastasis of Panc-1 cells after 5,7-DMF treatment were detected by scratch assay. Fox M1 protein The expression of EMT-related epithelial marker E-cadherin and interstitial marker N-cadherin protein in Panc-1 cells of human pancreatic cancer was detected by Western blot. Results: 5,7-DMF significantly inhibited the invasion and metastasis of Panc-1 cells in a concentration-dependent manner. The expression of Fox M1 was significantly down-regulated by 5,7-DMF in pancreatic cancer cells. Fox M1 si RNA was transfected into pancreatic cancer cells, and the expression of EMT-related molecules E-cadherin increased, while the expression of N-cadherin decreased compared with the control group All have statistical significance. CONCLUSION: 5,7-dimethoxyflavone can reverse the epithelial-mesenchymal transition of pancreatic cancer cells, which may be one of the important mechanisms by down-regulating Fox M1 level. However, its intrinsic molecular mechanism needs to be further explored.