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Fig. 2 | Journal of Experimental & Clinical Cancer Research

Fig. 2

From: MiR-455-5p suppresses PDZK1IP1 to promote the motility of oral squamous cell carcinoma and accelerate clinical cancer invasion by regulating partial epithelial-to-mesenchymal transition

Fig. 2

PDZK1IP1 is a potential target gene of miR-455-5p. A Western blotting of OEC-M1 and HSC-3 cells transfected with pLe-miR-455-5p (and controls). β-actin was used as a loading control. B, C Association between the expression of miR-455 and EMT (B) score or SNAI2 (C) in the TCGA head and neck squamous cell carcinoma database. D Venn diagram of predicted target genes of miR-455-5p. E Kaplan–Meier analysis revealed that high expression of PDZK1IP1 is associated with higher rates of overall survival in patients with HNSCC. F PDZK1IP1 expression of tumor samples with different histological differentiation. G PDZK1IP1 expression of tumor samples with different patterns of pathologic nodal extracapsular spread, according to the TCGA database. ECE: extracapsular extension. H Schematic of PDZK1IP1 3′-UTR sequence containing miR-455-5p binding site and the mutant type of PDZK1IP1 3′-UTR sequence. I Relative miR-455-5p and PDZK1IP1 mRNA expression in SAS cells transfected with miR-455-5p mimics and controls. J Western blotting revealed MAP17 protein expression in OEC-M1 cells transfected with miR-455-5p mimics and inhibitors (and controls). K Relative miR-455-5p expression in luciferase activity assay. L Wild type or mutant 3′-UTR of PDZK1IP1 in luciferase activity assay. **p < 0.01, ***p < 0.001, ****p < 0.0001 by Student’s t test

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