Fig. 7: Linc00665 upregulates AKR1B10 by competitively binding to miR-98. | Cell Death & Disease

Fig. 7: Linc00665 upregulates AKR1B10 by competitively binding to miR-98.

From: Long non-coding RNA linc00665 promotes lung adenocarcinoma progression and functions as ceRNA to regulate AKR1B10-ERK signaling by sponging miR-98

Fig. 7

a Correlation between miR-98 and linc00665 or AKR1B10 expression in 80 LUAD samples. b Relative miR-98 expression in A549 and H1299 cells following linc00665 knockdown or overexpression. c Relative linc00665 or AKR1B10 expression in A549 and H1299 cells after transfection with miR-98 mimics. d Putative binding sites of miR-98 to linc00665/AKR1B10, and schematic of wild-type and mutant pmirGLO-linc00665/pmirGLO-AKR1B10 constructs. e miR-98 mimics or mimics NC and pmirGLO-linc00665-WT or pmirGLO-linc00665-MUT were co-transfected into 293T, A549, and H1299 cells. Luciferase activity was detected 24 h after transfection using the dual-luciferase assay. f miR-98 mimics or mimics NC and pmirGLO-AKR1B10-WT or pmirGLO-AKR1B10-MUT were co-transfected into 293T, A549, and H1299 cells. Luciferase activity was detected 24 h after transfection using the dual-luciferase assay. g, h Biotin-labeled RNA pull down assays were performed to confirm the binding of linc00665 with miR-98 in A549 and H1299 cells. A significant amount of linc00665 and miR-98 were observed in linc00665-probe pulled down pellets. i Expression of AKR1B10 and GAPDH protein in A549 and H1299 cells after transfection with miR-98 mimics, miR-98 inhibitors, or linc00665 overexpression plasmid. NC negative control, NS not significant, LUAD, lung adenocarcinoma; *p < 0.05, **p < 0.01, ***p<0.001.

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