Effect Of 8-Bromo-7-Methoxy Chrysin On IL-6 Induced EMT In Small Cell Lung Cancernci-446 Cell Line

Objective:1.To study the effect of IL-6 on epithelial mesenchymal transition(EMT)in human small cell lung cancer NCI-H446 cells.2.To demonstrate whether IL-6 activates STAT3 signaling pathway in NCI-H446 cells.3.To determine whehter 8-bromo-7-methoxy chrysin(BrMC)inhibits IL-6-induced EMT inNCI-H446 cells.Methods:1.Human small cell lung cancer cell line NCI-H446 was cultured in vitro.2.PCR analyzedmRNA expression levels of IL-6 receptor(IL-6R)and Inhibitor of Apoptosis Protein(IAP)of NCI-H446 cells。3.Phase contrast microscope was used toobserve EMT cell morphologyalteration of NCI-H446 cells induced by IL-6.4.Western blot analyzed the effect of IL-6 on the protein expression levels of STAT3,p-STAT3,E-cadherin and N-cadherin in NCI-H446 cells.5.Western blot analyzed the effect of BrMC on EMT phenotype,expression of STAT3,p-STAT3,E-cadherin,N-cadherin protein in NCI-H446 cellsafter the activation of IL-6.Results:1.IL-6 induced EMT in NCI-H446 cellmorphology:form oval or round into spindle,polygons,and the pseudopodia.2.IL-6 significantly up-regulated the expression of p-STAT3 and N-cadherin(P < 0.05),but down-regulated E-cadherin protein expression(P < 0.05).3.BrMC inhibited IL-6-induced EMT in NCI-H446 cells.4.BrMC down-regulated the expression of STAT3、p-STAT3 and N-cadherin(P < 0.05),but the expression of E-cadherin was up-regulated by BrMC(P < 0.05).Conclusion:1.BrMC could significantly inhibit the IL-6-induced EMT phenotype of human small cell lung cancer NCI-H446 cells in vitro.2.The mechanisms how BrMC inhibits the EMT of NCI-H446 cells may be related to the down-regulation of p-STAT3.