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Fig. 5 | Biology Direct

Fig. 5

From: Transcription factor KLF15 inhibits the proliferation and migration of gastric cancer cells via regulating the TFAP2A-AS1/NISCH axis

Fig. 5

TFAP2A-AS1 is positively regulated by transcription factor KLF15. A UCSC and JASPAR were used to predict the potential mRNA, SOX12, FOXq1, ZNF740, KLF15, ZNF281 and IRF3, and their binding sites of TFAP2A-AS1 promoter. B QPCR was used to evaluate the overexpression efficiency of pcDNA3.1-SOX12, pcDNA3.1-FOXq1, pcDNA3.1-ZNF740, pcDNA3.1-KLF15, pcDNA3.1-ZNF281 and pcDNA3.1-IRF3 in AGS cells. C Dual luciferase reporter assay was conducted to verify the interaction between TFAP2A-AS1 promoter and all the candidates in AGS cells. D QPCR was conducted to evaluate the expression of KLF15 in AGS, NUGC4 and GES-1 cells. E, F Dual luciferase reporter and ChIP assays verified the interaction between TFAP2A-AS1 promoter and KLF15 in AGS cells. G QPCR detected the expression of TFAP2A-AS1 after the overexpression of KLF15 in AGS cells. H, I EdU and transwell assays were implemented in AGS cells after the transfection of pcDNA3.1, pcDNA3.1-KLF15, pcDNA3.1-KLF15 + sh-NC or pcDNA3.1-KLF15 + sh-TFAP2A-AS1-1. The statistical analysis for B, F, G was student’s t-test, for C was two-way ANOVA, and for D, E, H, I, J was one-way ANOVA. β-actin was used as the internal reference for gene expression analysis. **P < 0.01

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