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Fig. 6 | Journal of Translational Medicine

Fig. 6

From: MYBL2-induced PITPNA-AS1 upregulates SIK2 to exert oncogenic function in triple-negative breast cancer through miR-520d-5p and DDX54

Fig. 6

PITPNA-AS1 increased SIK2 mRNA stability via recruiting DDX54. A SIK2 mRNA stability in HCC1937 and MDA-MB-468 cells transfected sh-PITPNA-AS1#1 or sh-NC after treating with Actinomycin D was detected by RT-qPCR. B Four common RBPs for PITPNA-AS1 (CLIP Data ≥ 2) and SIK2 (CLIP Data ≥ 5) were predicted by starBase. C The binding capacity of PITPNA-AS1 to DDX54, FMR1, IGF2BP1 or IGF2BP2 was detected by RNA pull down assay. D Efficiency of silencing of DDX54 in HCC1937 and MDA-MB-468 cells was identified via RT-qPCR and western blot. E Stability of SIK2 mRNA in transfected cells treated with actinomycin D for 0, 4, 8, 12 h was evaluated by RT-qPCR. F The interaction of DDX54 protein with PITPNA-AS1 or SIK2 mRNA was verified through RIP assay. G RIP assay demonstrated the changes in the binding of DDX54 protein to SIK2 mRNA upon PITPNA-AS1 knockdown. H DDX54 expression at the mRNA and protein levels after silencing PITPNA-AS1 was measured by RT-qPCR and western blot. I RT-qPCR and western blot verified the overexpression efficiency of DDX54. J RT-qPCR and western blot analyses of SIK2 expression in HCC1937 and MDA-MB-468 cells transfected with indicated plasmids. **p < 0.01, ***p < 0.001

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