Fig. 4

H1FX-AS1 promoted DACT1 expression via sponging miR-324-3p. The schematic representation of the potential binding sites of miR-324-3p in the 3′ UTR of DACT1 predicted by targetscan (a), which was further confirmed by the dual-luciferase reporter assay of the SiHa (b, left panel) and HeLa (b, right panel) transfected by the WT or mutated DACT1-3′ UTR reporter with or without co-transfection of miR-324-3p; the mRNA (c) and the protein (d, images: left panel; quantification: right panel) expression levels of DACT1 in the SiHa and HeLa cells after miR-324-3p was silenced (miR-324-3p mimics) or over-expressed (miR-324-3p mimics); the mRNA (e) and the protein (f, images: left panel; quantification: right panel) expression levels of DACT1 in the SiHa and HeLa cells after H1FX-AS1 over-expression with or without miR-324-3p co-transfection; g the relative expression levels of DACT1 in paired CC and nearby normal tissues from 50 patients (same samples as in Fig. 1c, f) detected by RT-qPCR; h Pearson correlation analysis of the associations between DACT1 with H1FX-AS1 (left panel) and miR-324-3p (right panel) in the CC tissues from 50 CC patients (same samples as in Fig. 1c, f). **p < 0.01