Fig. 7.

CircMKLN1 promotes EMT by upregulating the expression of the miR-26a/b target CDK8. a Predicted targets combined with miR-26a/b. b The expression of predicted targets combined with miR-26a/b in the TGF-β1 group. *p < 0.05 vs. the control group. c Schematic of miR-26a/b combined with CDK8. d Luciferase assays of HEK293 cells co-transfected with a scrambled control, miR-26a/b mimic, and a luciferase reporter plasmid containing wild-type CDK8. *p < 0.05 vs. the CDK8 WT group. e The level of CDK8 protein in mouse lung tissues with inhibition of circMKLN1 expression. β-actin was used as the endogenous control. *p < 0.05 vs. the control group, #p < 0.05 vs. the AAV-vector + BLM group. f, g The level of CDK8 protein in A549 cells with regulation of circMKLN1 expression. β-actin was used as the endogenous control. *p < 0.05 vs. the si-NC/vector group, #p < 0.05 vs. the si-NC/vector + TGF-β1 group. h, i The levels of CDK8 and EMT-related indicators (E-cadherin, α-SMA and vimentin) after cotransfection of circMKLN1 siRNA and miR-26a/b inhibitor in TGF-β1-treated A549 cells. β-actin was used as the endogenous control. *p < 0.05 vs. the NC + TGF-β1 group, #p < 0.05 vs. the si-circMKLN1 + TGF-β1 group. j, k The levels of CDK8 and EMT-related indicators (E-cadherin, α-SMA and vimentin) after cotransfection of the circMKLN1 plasmid and miR-26a/b mimic in TGF-β1-treated A549 cells. β-actin was used as the endogenous control. *p < 0.05 vs. the vector + TGF-β1 group, #p < 0.05 vs. the circMKLN1 + TGF-β1 group