Fig. 4

LncRNA like NMRK2 mRNA upregulated the expression of SLC19A2 by adsorbing miR-26b and miR-181a. A The enrichment of AGO2 on NMRK2, miR-26b, or miR-181a was assessed by RIP assay. Rabbit IgG was used as a negative control. B UOK109 cells were transfected with control, miR-26b or miR-181a mimic RNA. The enrichment of AGO2 on NMRK2 was assessed by RIP assay. Rabbit IgG was used as a negative control. C UOK109 cells were transfected with lentivirus shRNA (NC) or shRNA (NMRK2). The expression of the target genes of miR-26b and miR-181a were detected by q-PCR. 18S rRNA was used as the reference gene. D Schematic of binding sites mutation or deletion between the 3’-UTR of SLC19A2 and miR-26b/miR-181a. E–G HEK293T cells were co-transfected with the reporter plasmids containing the wild, mutated, or deleted binding sites between the 3’-UTR of SLC19A2 and miR-26b/miR-181a and 0 nM or 40 nM miR-26b/miR-181a mimic RNA. The luciferase activity in each group was measured with a Dual-Luciferase Reporter Assay Kit. H-J UOK109 cells were transfected with lentivirus shRNA (NC) or shRNA (NMRK2) and reporter plasmids containing the wild, mutated, or deleted binding sites between the 3’-UTR of SLC19A2 and miR-26b/miR-181a. The luciferase activity in each group was measured with a Dual-Luciferase Reporter Assay Kit. Data are presented as the mean ± SEM. *P < 0.05, **P < 0.01, ***P < 0.001