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. 2021 Oct 13;22(20):11020. doi: 10.3390/ijms222011020

Figure 3.

Figure 3

miR143-3p targeted BIRC2 in cervical cancer cells. (A) Putative target site of miR143-3p at the 3′-UTR of BIRC2. (B) Effect of miR143-3p on the luciferase activity of wild-type Luc-BIRC2-3′-UTR (Wt-Luc-BIRC2-3′-UTR) and mut-Luc-BIRC2-3′-UTR (Mut-Luc-BIRC2-3′-UTR). HeLa-S3 cells were transfected with Luc-BIRC2-3′-UTR along with miR143-3p or scrambled as a control miR for 48 h. Data are presented as the means ± standard errors of relative luciferase activity, normalized to those of scrambled controls from three independent experiments. (C) Suppression of BIRC2 mRNA through miR143-3p or transfection with anti-miR-143-3p increased mRNA expression of BIRC2, as detected through real-time qPCR conducted using BIRC2 and GAPDH primers. GAPDH was used as an internal control. (D) miR143-3p suppressed the expression of BIRC2 protein, and the suppression of endogenous miR-143-3p with anti-miR-143-3p increased BIRC2 protein levels (as determined through immunoblotting with β-actin as a loading control). (E) HeLa-S3 cells were transiently transfected with miR143-3p or anti-miR-143-3p for 7–14 days. Colony formation was analyzed through the clonogenic assay. * p < 0.05 relative to controls.