ANGPTL4通过调节上皮间充质转化促进舌癌细胞转移的分子机制研究

Molecular mechanism of ANGPTL4 promoting the metastasis of tongue cancer cells by regulating epithelial-mesenchymal transition

目的:探究血管生成素样蛋白4(ANGPTL4)在舌癌进展及淋巴结转移中的分子机制,以期为舌癌的治疗提供新的分子靶点。方法:使用小干扰RNA(siRNA)沉默Tca8113细胞中的ANGPTL4基因,实时荧光定量PCR检验转染效率,通过CCK-8、Transwell和划痕实验确定ANGPTL4沉默后Tca8113细胞的生物学行为变化;实时荧光定量PCR和Western blot实验检测细胞上皮间充质转化(EMT)相关指标的表达变化。结果:与空白对照组相比,siRNA沉默ANGPTL4后,细胞的增殖显著降低(P<0.01),且细胞迁移能力明显减弱(P<0.05)。与EMT相关的钙黏蛋白(E-cadherin)上调,波形蛋白(Vimentin)、盘装结构域受体1(DDR1)、锌指结合蛋白(ZEB-1)的表达下调。结论:ANGPTL4可以降低Tca8113细胞间黏附,促进Tca8113细胞的迁移和EMT,ANGPTL4可为舌癌淋巴结转移的潜在靶点。

Objective:To explore the molecular mechanism of ANGPTL4 in the progression and lymph node metastasis of tongue cancer,in order to provide a new molecular target for the treatment of tongue cancer.Methods:The ANGPTL4 gene in tongue cancer cells was silenced by small interfering RNA(siRNA).The transfection efficiency was tested by qRT-PCR.The biological behavior of tongue cancer cells after ANGPTL4 silencing was determined by CCK-8,Transwell and scratch experiments.The expressions of epithelial-to-mesenchymal transition(EMT)related markers were detected by reverse transcription polymerase chain reaction and Western blotting.Results:After silencing ANGPTL4 by siRNA,the proliferation was significantly reduced(P<0.01)and migration ability of tongue cancer cells was weakened(P<0.05).The expression of downstream related genes of EMT,E-cadherin was up-regulated and Vimentin,DDR1,ZEB-1 were down-regulated.Conclusions:ANGPTL4 can enhance the adhesion between tongue cancer cells,thereby reducing the migration and epithelial-mesenchymal transition of tongue cancer cells.ANGPTL4 may be a potential target for lymph node metastasis of tongue cancer.