Fig. 5
miR-124 also participates in inhibiting the oncogenic KITENIN complex by DKC1125. a Modulated miRNA under KITENIN overexpression and effects of DKC1125. Changes in miRNA in Caco2 cells transfected with empty vector (EV) or KITENIN, and the effects of DKC1125 on these cells, were examined by using the Pathway-focused miScript miRNA cancer pathway. After array processing and normalization of raw array data, we identified seven differentially expressed miRNAs whose levels were changed under KITENIN overexpression but restored after treatment with DKC1125 (0.5 μM). miRNAs identified by array were analyzed again by miScript primer assay, which detected the expression of miRNAs under the same conditions as the array. Data were represented as mean ± SEM (n = 3). The asterisk indicates a significant difference between Caco2/EV cells and vehicle-treated Caco2/KITENIN-V5 cells (*P < 0.05; **P < 0.01), and a significant difference in Caco2/KITENIN-V5 cells after treatment with DKC1125 (#P < 0.05; ##P < 0.01). b Effect of DKC1125 on miR-124-3p in KITENIN-overexpressing cells was dependent on the level of KSRP. Caco2 cells stably transfected with empty vector (EV) or KITENIN-V5 were transfected with si-NC or si-KSRP, and then treated with vehicle or DKC1125 (0.5 μM). miR-124-3p transcript levels were compared among groups (right panel). c Treatment with DKC1125 increases KSRP-bound miR-124-3p. The anti-KSRP antibody-bound miR-124-3p was examined by RNA immunoprecipitation (RIP) assay in empty vector (EV) or KITENIN-V5-transfected Caco2 cells, which were treated with vehicle or DKC1125 (0.5 μM). d Treatment of DKC1125 increases mature miR-124-3p. Caco2 cells stably transfected with empty vector (EV) or KITENIN-V5 were treated with vehicle or DKC1125 (0.5 μM). The unprocessed pri-miR124-3p and mature miR-124-3p were detected and compared among groups