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Fig. 6 | Journal of Translational Medicine

Fig. 6

From: The permissive role of TCTP in PM2.5/NNK-induced epithelial–mesenchymal transition in lung cells

Fig. 6

MiR-125a-3p inhibited PM2.5- and NNK-induced EMT via down-regulating TCTP. a Effect of miR-125a-3p on PM2.5- or NNK-induced TCTP and vimentin expression. After Bet1A or NCI-H23 cells were treated with PM2.5 or NNK for 28 days, the cells were transfected with miR-125a-3p mimic or miR-NC control respectively, cells were incubated for 24 h. The levels of TCTP and vimentin were determined. The equal loading was confirmed by measuring actin protein. The quantification of protein was carried out by densitometry analysis, and the result was presented by the relative intensity of the control condition based on actin normalization for total protein. The relative intensity of protein bands was summarized by column figure. The values indicate the mean ± SD of three independent experiments. **p < 0.01 vs each control condition; and ##p < 0.01 vs miR-NC + PM2.5 or miR-NC + NNK respectively. b Effect of miR-125a-3p on PM2.5- or NNK-induced cell migration. Bet1A cells and NCI-H23 cells were treated with PM2.5 or NNK for 28 days. Then the cells were transfected with miR-125a-3p mimic or miR-NC control respectively. Wound-healing assay were then performed. Images were taken using phase contrast microscope (Nikon) (scale bar, 20 μm). The values indicate the mean ± SD of three independent experiments, **p < 0.01 vs miR-NC control; ##p < 0.01 vs miR-NC + PM2.5 or miR-NC + NNK respectively. c Effect of miR-125a-3p on PM2.5- or NNK-induced cell invasion. Cells were treated by PM2.5 or NNK for 28 days. Then the cells transfected with miR-125a-3p mimic or miR-NC control respectively for invasion assay. Images were taken using phase contrast microscope (Nikon) (scale bar, 20 μm). The numbers of invading cells in four randomly selected high-power fields (HPF) were counted and the average number of cells in a HPF was calculated. The values indicate the mean ± SD of three independent experiments. **p < 0.01 vs miR-NC control; ##p < 0.01 vs miR-NC + PM2.5 or miR-NC + NNK respectively. d Schematic of the role of TCTP in promoting PM2.5- and NNK-induced EMT during lung carcinogenesis. Upon PM2.5 or NNK stimulation, the TCTP specific microRNA, namely miR-125a-3p, was down regulated, which in turn increased the expression of TCTP. Then TCTP promoted PM2.5- or NNK-induced EMT via up-regulating vimentin

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