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Fig. 4 | BMC Cancer

Fig. 4

From: Oncogenic role of ALX3 in cervical cancer cells through KDM2B-mediated histone demethylation of CDC25A

Fig. 4

CDC25A is activated by the transcription factor ALX3. A potential transcription factors that may bind to the promoter region of CDC25A predicted on JASPAR; B conservative binding sites of ASCL1, ARNT and ALX3; C correlations between CDC25A expression and ASCL1, ARNT or ALX3 predicted on GEPIA database; D binding relationship between ALX3 and the CDC25A promoter validated by the ChIP-qPCR; E a diagram for the constructed pGL3-Enhancer-promoter; F binding relationship between ALX3 and the CDC25A promoter validated through a luciferase reporter gene assay; G ALX3 expression in TCGA-CESC in the GEPIA database; H-I, mRNA (H) and protein (I) expression of ALX3 in CSCC cell lines (C33A, Caski, HeLa and ME180) and in normal cervical epithelial cells (PCS480) determined by RT-qPCR and western blot analysis, respectively; J-K mRNA (J) and protein (K) expression of ALX3 and CDC25A in ME180 and C33A cells after ALX3 shRNA transfection examined by RT-qPCR and western bot analysis, respectively. Data were presented as the mean ± SD from three independent experiments. Data were analyzed by one-way (F, H, I, J and K) or two-way (D) ANOVA followed by Tukey’s multiple comparison test. In panel D, **p < 0.01 vs. IgG; in panel F, **p < 0.01 vs. 0 ng pCDNA3.1-ALX3; in panels H and I, **p < 0.01 vs. PCS-480 cells; in panels J and K, **p < 0.01 vs. sh-NC. All cellular experiments were performed in triplicates and three duplicated wells were set

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