Fig. 4: 1700020I14Rik interacted with miR-34a-5p by both directly targeting and Ago2-dependent manner. | Cell Death & Disease

Fig. 4: 1700020I14Rik interacted with miR-34a-5p by both directly targeting and Ago2-dependent manner.

From: LincRNA 1700020I14Rik alleviates cell proliferation and fibrosis in diabetic nephropathy via miR-34a-5p/Sirt1/HIF-1α signaling

Fig. 4

a Predicted binding sites of miR-34a-5p of four species on 1700020I14Rik transcript. The red part of the column indicates the potential binding sites. b The inverse expression of 1700020I14Rik and miR-34a-5p in MCs cultured in high glucose or low glucose medium was assessed by qRT-PCR. c The expression of miR-34a-5p regulated by 1700020I14Rik plasmid or its siRNA was measured by qRT-PCR. d The expression of miR-34a-5p regulated by miR-34a-5p mimics and inhibitor was measured by qRT-PCR. e The expression of 1700020I14Rik regulated by miR-34a-5p mimics or inhibitor was detected by qRT-PCR. Data suggested that 1700020I14Rik had an opposite expression comparing with miR-34a-5p in MCs. f Dual-luciferase reporter assay was performed to measure the luciferase activity in cells co-transfected with miR-34a-5p and luciferase reporters containing 1700020I14Rik (1700020I14Rik wt), mutant transcript (1700020I14Rik mut), or miR-34a-5p inhibitor (as positive control, PC). These results indicated that there was direct interaction between 1700020I14Rik and miR-34a-5p. Data were presented as the relative ratio of firefly luciferase activity to renilla luciferase activity. g RIP assay was performed in MCs cultured in high glucose, followed by qRT-PCR to detect 1700020I14Rik and miR-34a-5p associated with AGO2. Data were represented as the mean ± SD of three independent experiments. *p < 0.05, **p < 0.01, and ***p < 0.001, n.s: no statistical significance

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