KRT6A介导Wnt/β-catenin信号通路调节上皮-间质转化促进非小细胞肺癌A549细胞抗辐射OA北大核心CSTPCD

Objective To explore the effect of KRT6A on radiation resistance in non-small cell lung cancer A549 cells and its mecha-nism of action.Methods The radiation-resistant A549(A549-RR)cells were induced and established.The successful construction of the cells were performed using the Cell Counting Kit 8(CCK-8)method,plate clone-formation experiments,and flow cytometry.Western blot-ting was used to detect the expression of KRT6A in A549 and A549-RR cells.A549-RR cells were divided into the sh-NC,sh-KRT6A,sh-KRT6A+ov-NC,and sh-KRT6A+ov-β-catenin groups.The expression of KRT6A;β-catenin;and epithelial-mesenchymal transition(EMT)-related proteins E-cadherin,N-cadherin,vimentin,Snail,and Slug were detected by Western blotting.The CCK-8 assay,plate clone-formation experiments,and flow cytometry were used to determine the radiation resistance of the cells.Results A549-RR cells were successfully cultured.and KRT6A expression was upregulated in A549-RR cells compared to A549 cells.Knocking down KRT6A reduced the proliferative activity and clonogenic ability of A549-RR cells;increased the apoptosis rate;upregulated the expression of E-cadherin protein;and downregulated N-cadherin,vimentin,Snail,Slug,andβ-catenin protein expression.Overexpression ofβ-catenin reversed the inhibitory effect of KRT6A knockdown on EMT and radiation resistance in A549-RR cells.Conclusion KRT6A is upregu-lated in A549-RR cells,and knocking down KRT6A reduces the radiation resistance of A549-RR cells,which may be related to the induc-tion of EMT by activation of the Wnt/βcatenin signaling pathway.