Lumican调控FAK信号通路对胃癌AGS细胞增殖、侵袭和迁移的影响

The effect of Lumican on the proliferation,invasion and migration of grastric cancer AGS cells through regulating the FAK signaling pathway

目的:探讨光蛋白聚糖(lumican)调控FAK信号通路对胃癌AGS细胞增殖、侵袭和迁移的影响。方法:采用实时荧光定量PCR(qPCR)法检测胃癌组织与正常胃组织中lumican的表达。通过转染小干扰RNA(siRNA)或过表达(OE)质粒下调或上调胃癌AGS细胞中lumican的表达,EDU检测细胞增殖,Transwell检测细胞侵袭、迁移,Western blotting检测lumican、粘着斑激酶(FAK)、磷酸化(p-)FAK蛋白表达量。结果:胃癌组织中lumican蛋白表达量明显高于正常胃组织(P<0.05)。与siRNA阴性对照(NC)组相比,siRNA组AGS细胞增殖、侵袭及迁移能力显著降低(P<0.05),而OE组AGS细胞增殖、侵袭及迁移能力明显增强(P<0.05);siRNA组FAK和p-FAK蛋白表达量下降(P<0.05),而OE组FAK和p-FAK相关蛋白表达量升高(P<0.05)。结论:Lumican在胃癌组织中的表达增强,其可能通过激活FAK/p-FAK通路促进胃癌AGS细胞侵袭、迁移及增殖。

Objective:To explore the effect of Lumican on the proliferation,invasion and migration of gastric cancer AGS cells by regulating the FAK signaling pathway.Methods:Real-time fluorescence quantitative PCR(qPCR)was used to detect the lumicanexpression in gastric cancer and normal gastric tissues.The expression of lumican in gastric cancer AGS cells was up-regulated or down-regulated by overexpression of plasmid or siRNA transfection.EDU was used to detect cell proliferation,and transwell was used to detect cell invasion and migration.The protein expression levels of lumican,focal adhesion kinase(FAK)and phosphorylated(p-)FAK were detected by westernblotting.Results:The expression of lumican in gastric cancer tissues was significantly higher than that in normal gastric tissues(P<0.05).Compared with the negative control group,the proliferation,invasion and migration of AGS cells in the lumican siRNA silenced group were significantly decreased(P<0.05),while the proliferation,invasion and migration of AGS cells in the lumican overexpressed group were significantly increased(P<0.05).The expressions of FAK and p-FAK in AGS cells were decreased in the lumican siRNA group(P<0.05),while the expressions of FAK and p-FAK were increased in the lumican overexpression group(P<0.05).Conclusion:The expression of lumican in gastric cancer tissues is enhanced.Lumican may promote the invasion,migration and proliferation of gastric cancer AGS cells by the activation of FAK/p-FAK pathway.