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Fig. 6 | Journal of Experimental & Clinical Cancer Research

Fig. 6

From: Ambient fine particulate matter inhibits 15-lipoxygenases to promote lung carcinogenesis

Fig. 6

miRNAs downregulated the expression of 15-LOX1 and 15-LOX2 in PM2.5- or NNK-induced lung carcinogenic cells. Predicted binding sites of miRNAs on 15-LOX1 3′-UTR region (a); and on 15-LOX2 3′-UTR region (c). The alignment of miR-18a, miR-203 with two predicted binding sites of 15-LOX1 3′-UTR were shown; The alignment of miR-17, miR-20a, miR-20b, miR-93, miR-106a, miR-106b, and miR590-3p with three predicted binding sites of 15-LOX2 3′-UTR were shown. b miRNAs targeted on 15-LOX1 3′-UTR region were upregulated; and (d) miRNAs targeted on 15-LOX2 3′-UTR region were upregulated in PM2.5- or NNK-induced lung carcinogenic cells. Bet1A and NCI-H23 cells were treated with PM2.5 or NNK for 4 h, 15 days, and 28 days. Total RNA were extracted for real-time PCR assay (n = 3, *p < 0.05 and **p < 0.01when compared each PM2.5 or NNK treated condition with the control cells.). e 15-LOX1 and 15-LOX2 transcriptional activity was downregulated by PM2.5 or NNK. Bet1A or NCI-H23 cells were transfected with luciferase reporter constructs, pGL3–15-LOX1 3′-UTR or pGL3–15-LOX2 3′-UTR for 24 h, the pGL3 basic vector and the pGL3 control were used as negative and positive controls, respectively, followed by PM2.5 or NNK treatment for 6 h. Reporter assays were performed using the Dual-luciferase assay system, normalized for transfection efficiency by co-transfected Renilla luciferase (n = 3, *p < 0.05 and **P < 0.01, compared with the cells transfected with 15-LOX1/2 3′-UTR alone)

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