Effect Of Down-regulation Of Cofilin Expression By ShRNA On Lung Cancer Cell Migration,Invasion And Cytoskeleton

Objective To explore the expression of Cofilin protein in lung cancer cell lines,and the association between Cofilin protein expression and migration,invasion,and microfialmant cytoskeleton system.Moreover,we further evaluate the relationship with the expression of Cofilin protein and clinicopathological parameters,metastasis of human lung cancer tissues.By this study,we try to provide certain theoretical basis for prognosis judgment and new target therapy in lung cancer.Method The expression of Cofilin protein in lung cancer cell lines(95D,801D,PG,95C,A549,BEAS-2B)was detected by Western blotting.Furthermore,Cofilin protein was detected by immuno-histochemical staining SP technique in tumor tissues from 100 lung cancer cases and in normal lung tissues from 30 patients.By shRNA cell transfection,the scratch test,transwell test,fluorescence microscopyand other technology detect the biological behaviour of lung cancer cells which has been down-regulated Cofilin protein.Results 1.The expression levels of Cofilin protein in 801D,95D and PG celllines were significantly up-regulated in 95C,A549 and BEAS-2B cell lines,which may be associated with lung cancer metastasis.2.The expression levels of Cofilin protein in lung cancer tissues were significantly up-regulated in normal lung tissues.Furthermore,the up-regulation of Cofilin expression was significantly correlated with lymph node metastasis(X2=10.256,P<0.01),but not correlated with age,sex,tumor size,histological type,clinical TNM system and pathological grading(P>0.05).3.Down-regulation of Cofilin specific inhibited the cell migration and invasion.It also induced rearrangements of the actin cytoskeleton.Conclusion:Cofilin played an important role in the tumorigenicity and metastasis of lung cancer cells,which will provide certain theoretical basis for prognosis judgment.Therefore,we proposed that Cofilin could be a potential molecular target of gene therapy in lung cancer cells,Which provide a theoretical basis for clinical tumor targeted therapy.