Fig. 4
From: The permissive role of TCTP in PM2.5/NNK-induced epithelial–mesenchymal transition in lung cells
MicroRNAs targeted on TCTP were down-regulated by PM2.5 and NNK. a Predicted binding sites of miRNAs on TCTP 3′-UTR region. All the individual candidate miRNAs were reported, namely miR-27a, miR-27b, miR-33a, miR-33b, miR-128, miR-125a-3p, miR-371a-5p, miR-365 and miR-425. The predicted binding sites of miRNAs on TCTP 3′-UTR were shown. b Predicted binding sites of miR-125a-3p, miR-371a-5p, and miR-425 on TCTP 3′-UTR region. The alignment of miR-125a-3p, miR-371a-5p, and miR-425 with four predicted binding sites of TCTP 3′-UTR were shown. c MiRNAs targeted on TCTP 3′-UTR region were down-regulated by PM2.5 and NNK. Bet1A and NCI-H23 cells were treated with PM2.5 or NNK for 15 days and 28 days respectively. Total RNAs were extracted for real-time PCR assay. The values indicate the mean ± SD of three independent experiments (**p < 0.01 vs control). d TCTP transcriptional activity was upregulated by PM2.5 or NNK. Bet1A cells and NCI-H23 cells were treated with PM2.5 or NNK for 28 days. Then cells were transfected with luciferase reporter constructs containing the pGL3-TCTP 3′-UTR and incubated for 24 h. The pGL3 basic vector and the pGL3 control were used as negative and positive controls respectively. Reporter assays were performed using the Dual-luciferase assay system, normalized for transfection efficiency by co-transfected Renilla luciferase. Data are expressed as mean ± SD of three independent experiments performed in triplicate (*p < 0.05 vs TCTP 3′-UTR)